Podcasts about natarajan

Enjoying the Ecommerce Coffee Break Podcast? Here are a few ways to grow your business: https://ecommercecoffeebreak.com/level-up/ ---In this episode, we continue our three-part miniseries on eCommerce search, focusing on the critical role of analytics and reporting in driving online retail success.  Host Claus Lauter welcomes back Arv Natarajan, Director of Product at GroupBy, to explore how robust data analysis can help eCommerce retailers make better decisions and improve their customer experience through AI-powered insights. Topics discussed in this episode:  How analytics drive eCommerce success through data-driven decisions. What role AI plays in transforming raw data into actionable insights. Why tracking search terms reveals vital customer intent patterns. How to pick the most important metrics for your online store. Why search vs browse behavior impacts different retail sectors. What null searches reveal about missed revenue opportunities. How GroupBy integrates with Shopify's native data collection. Why anonymous tracking delivers better personalization results. What makes an ideal analytics solution for merchants. How usage-based pricing works for stores of all sizes. Find the first episode of the mini series here:  https://ecommercecoffeebreak.com/future-of-ecommerce-search-ai/ Links & Resources Website: https://www.groupbyinc.com/integrations/shopify Shopify App Store: https://apps.shopify.com/groupby-ai-search-discovery LinkedIn: https://www.linkedin.com/in/arvnatarajan/ X/Twitter: https://x.com/groupbyinc  Get access to more free resources by visiting the show notes athttps://tinyurl.com/4wdh98kt MORE RESOURCESDownload the Ecommerce Conversion Handbook for store optimization tips at https://tinyurl.com/CRO-ebook Best Apps to Grow Your eCommerce Store: https://ecommercecoffeebreak.com/best-shopify-marketing-tools-recommendations/ Become a smarter online seller in just 7 minutes Our free newsletter is your shortcut to ecommerce success. Every Thursday. 100% free. Unsubscribe anytime. Sign up at https://newsletter.ecommercecoffeebreak.com Rate, Review & Follow Enjoying this episode? Help others like you by rating and reviewing my show on Apple Podcasts. Rate here: https://podcasts.apple.com/us/podcast/ecommerce-coffee-break-digital-marketing-podcast-for/id1567749422 Follow the podcast to catch all the bonus episodes I am adding. Do not miss out. Hit that follow button now!

Welcome to another episode of the CSCEN Podcast Key words: farming, micro-finance, climate change, & adaptation, debt-cycles, sustainability In this episode, CSCEN's Millie Cave speaks to special guest Dr Nithya Natarajan - Senior Lecturer at King's College London. Dr Natarajan shares her expertise and research insights on the challenges of unsustainable finance structures in Cambodia and India, the effects of climate change on farming communities and the potential influence of climate adaption policy. We would like to thank Dr Natarajan for joining us on the podcast. Want to find out more about her research? Please follow the links below: https://kclpure.kcl.ac.uk/portal/en/publications/depleted-by-debt-green-microfinance-over-indebtedness-and-social- https://kclpure.kcl.ac.uk/portal/en/publications/diffuse-drivers-of-modern-slavery-from-microfinance-to-unfree-lab-2 https://kclpure.kcl.ac.uk/portal/en/publications/diffuse-drivers-of-modern-slavery-from-microfinance-to-unfree-lab Disclaimer: The views, thoughts, and opinions expressed are the speaker's own and do not represent the views, thoughts, and opinions of the Civil Service Climate and Environment Network. The material and information presented here is for general information purposes only.

Enjoying the Ecommerce Coffee Break Podcast? Here are a few ways to grow your business: https://ecommercecoffeebreak.com/level-up/ ---In this first episode of our special mini-series on ecommerce search, Arv Natarajan, Director of Product at GroupBy Inc., explores how artificial intelligence is revolutionizing digital customer experiences.  From early keyword matching to today's sophisticated AI-powered solutions, Arv breaks down the transformation of search technology and its critical role in creating personalized shopping journeys. Topics discussed in this episode:  How early e-commerce search failed due to basic keyword matching. Why AI understands shopping intent vs just matching words. How search personalization works without compromising privacy. Why both search and browse experiences matter equally. What makes the perfect e-commerce search page layout. How visual search transforms product discovery. Why conversational AI revolutionizes complex shopping queries. What makes unified AI shopping assistants the future. How search analytics reveal hidden inventory issues. Why "revenue per search" is the only metric that matters. Links & Resources  Website: https://www.groupbyinc.com/integrations/shopify Shopify App Store: https://apps.shopify.com/groupby-ai-search-discovery LinkedIn: https://www.linkedin.com/in/arvnatarajan/ X/Twitter: https://x.com/groupbyinc  Get access to more free resources by visiting the show notes athttps://tinyurl.com/3fftw9mw MORE RESOURCESDownload the Ecommerce Conversion Handbook for store optimization tips at https://tinyurl.com/CRO-ebook Best Apps to Grow Your eCommerce Store: https://ecommercecoffeebreak.com/best-shopify-marketing-tools-recommendations/ Become a smarter online seller in just 7 minutes Our free newsletter is your shortcut to ecommerce success. Every Thursday. 100% free. Unsubscribe anytime. Sign up at https://newsletter.ecommercecoffeebreak.com Rate, Review & Follow Enjoying this episode? Help others like you by rating and reviewing my show on Apple Podcasts. Rate here: https://podcasts.apple.com/us/podcast/ecommerce-coffee-break-digital-marketing-podcast-for/id1567749422 And if you haven't yet, follow the podcast to catch all the bonus episodes I'm adding. Don't miss out—hit that follow button now!

934: Fraud is constantly evolving, but leveraging data accelerates understanding and adaptation to changes in the environment. In this episode of Technovation, Peter High interviews Prem Natarajan, EVP, Chief Scientist and Head of Enterprise AI at Capital One. Prem delves into how Capital One is leveraging AI to revolutionize financial services, with applications ranging from fraud detection to customer service enhancements. Discover how the company's vibrant tech culture and partnerships with academia fuel innovation, and learn why Prem believes diverse perspectives are critical in shaping the future of AI.

In this insightful episode, Santhoshi Natarajan from Zuddl shares her expertise on their unified event management platform.  Designed to streamline every phase of events, from conferences and webinars to field events and hybrid experiences, Zuddl empowers B2B companies with customizable solutions.  Discover how their purpose-built approach addresses event marketers' needs while ensuring a seamless attendee experience.

Mon, 09 Dec 2024 07:00:00 +0000 https://talkingtransporttransformation.podigee.io/44-sarayu-natarajan e0a4f273557486e93fb252bf20f862f8 In this episode of TTT – Talking Transport Transformation, we are joined by Sarayu Natarajan, founder of the Aapti Institute in India. Sarayu shares her expertise on the intersection of society, technology, and public policy, discussing how data and digital solutions can shape more equitable and inclusive urban mobility systems. Together, we explore: The role of digital solutions and AI in addressing mobility disparities, including the Gender Data Gap. The concept of Data Stewards and how they can ensure transparency, fairness, and accountability in the use of mobility data. The challenges and opportunities in building data-driven, gender-responsive transportation systems. Sarayu also emphasizes the importance of data governance and collaborative frameworks to make mobility systems more just and inclusive. Tune in to hear her unique perspectives and learn how technology can transform mobility for everyone. Learn more about her work with the Aapti-Institute Links Mobility of Care: Introducing New Concepts in Urban Transport Many thanks to Our TUMI Partners: ADB, BMZ, C40 Cities, CAF, GIZ, ICLEI, ITDP, KfW, SLOCAT, UN-Habitat, WRI Our Guest: Sarayu Natarajan LinkedIn Our Moderator Frederic Bocklet LinkedIn Max Bleß from audioBoutique for the sounddesign Sebastian Hofer from freifahrt for the concept and production support LINKS and INFORMATION about TUMI Twitter Facebook Youtube Website E-Mail: info@transformative-mobility.org 44 full no Transforma

Krishnakumar Natarajan, Co-founder at Mela Ventures, discusses his firm's AI investment thesis.

Arv is the Director of Product at GroupBy. He is a passionate entrepreneur currently responsible for product management. Arv has over eight years of experience in the oil and gas industry, including five years with WorleyParsons.In This Conversation We Discuss: [00:45] Intro[01:21] Driving revenue with better product discovery[02:40] Scaling search for retailers with high SKU counts[03:31] Adapting to modern, conversational search queries[05:58] Better product details for user-friendly browsing[08:30] Avoiding AI errors with human-guided review[09:55] Guiding users with smart sorting options[11:46] Product variations using smart automation[13:02] Shopper trust through respectful customization[14:09] Automating reorders with helpful reminders[15:05] Preventing bounce rates with smart stock management[16:32] Clear shipping times to boost purchase confidence[17:11] advanced analytics for more effective action[18:34] Using best-in-class apps as your brand grows[20:17] Recognizing evolving trends in ecommerce technology[21:24] Product search with AI-driven recommendations[23:01] GroupBy for enhancing your retail experienceResources:Subscribe to Honest Ecommerce on YoutubeProduct discovery platform powered by Google Cloud Vertex AI search for retail groupbyinc.com/Follow Arv Natarajan linkedin.com/in/arvnatarajan/If you're enjoying the show, we'd love it if you left Honest Ecommerce a review on Apple Podcasts. It makes a huge impact on the success of the podcast, and we love reading every one of your reviews!

Trechos de gravações em Satsangs. Swami Dayananda Saraswati ou Natarajan (1930 - 2015), foi um sannyasa, professor tradicional de Advaita Vedanta e fundador do Arsha Vidya Gurukulam e AIM For Seva. Swamiji nasceu em Manjakkudi no sul da Índia. Em 1953, morando e trabalhando em Chennai, conheceu Swami Chinmayananda, que se tornou um de seus mestres. Então, aprofundando-se no conhecimento de Vedanta e Sânscrito, em 1962 tornou-se um renunciante. Dayananda começou a ensinar às margens do rio Ganges, e em 1973 foi chamado para ensinar em Mumbai. Seus cursos, também ministrados em Inglês, abriram aos estudantes do Ocidente a oportunidade de acesso a este ensinamento. Swamiji viajou por toda a Índia ministrando cursos e palestras, e desde 1976 foi para os Estados Unidos, Canadá, Inglaterra, Suécia, Austrália, África do Sul, Brasil e Argentina. Em todos esses países, assim como na Índia, era conhecido por sua facilidade de comunicação e pela clareza e profundidade de seu conhecimento de Vedanta e da complexidade humana. Dayananda estabeleceu dois Ashrams na Índia, um em Rishikesh e outro em Coimbatore, e o Arsha Vidya Gurukulam, nos Estados Unidos. Nessas instituições, Swamiji era o principal professor. Nos cursos de Vedanta e Sânscrito o ensinamento é passado de mestre a discípulo, num fluir permanente, que tem como objetivo desdobrar a visão do “eu” como um Ser completo e livre. Saiba mais em: https://www.yoga.pro.br/meditacao-a-v... “O que é liberdade? Eu defino a liberdade de uma forma dupla: a liberdade do passado e a liberdade do conceito de passado, presente e futuro. Estes são dois tipos de liberdade. A liberdade do passado se refere a sua própria vida passada, ou seja, nesta vida, a sua infância e assim por diante. O passado de todos tem os seus próprios problemas e esses problemas afetam a pessoa no presente. O que eu enfrento agora, neste momento, não é visto objetivamente, pois é sempre reprimido, condicionado, imbuído de preconceito e distorcido pelo meu próprio passado. A liberdade desse passado significa a liberdade do meu passado psicológico. A liberdade do passado psicológico de alguém é uma liberdade relativa, descrito na Gita como a liberdade da pressão dos próprios gostos e aversões”. Swami Dayananda. “A liberdade definitiva deve ser necessariamente centrada no ‘eu', já que eu sou aquele que está preso e também sou aquele que tem que se libertar. Essa liberdade já é intrínseca ao Ser ou ela não seria possível de modo algum. Se ela é intrínseca ao Ser, então a escravidão nasce da auto-ignorância. A remoção da ignorância é a liberdade, Moksha”. Swami Dayananda. “Numa estrada esburacada, quando você vai numa van sem amortecedores, você absorve o impacto dos buracos. Ora, acontece que seu corpo não foi feito para absorver esse impacto. Você precisa ter amortecedores que lhe protejam das coisas do mundo. Deveria haver um fator que possa isolar você de se ferir, de ser afetado e sofrer pelo que acontece à sua volta. Esse sofrimento acontece porque não há uma compreensão básica dos fatos, do que significa estar vivo, do que é o mundo, o que são as pessoas e o que são as relações. Você pode sim, ter esses amortecedores, esse isolamento que lhe ajude a viver em paz. Com responsabilidade. Quando você dirige um carro precisa ter cuidado para não bater em ninguém, pois bater nos demais ou nos carros dos demais significa igualmente bater seu próprio carro. Precisamos, assim, aprender a viver a vida sem ferir os demais e sem sermos feridos pelo que outrem possam fazer. Isso é responsabilidade”. Swami Dayananda. Música: Zerofuturism - Rays Of Light Pierce The Darkness (   / lzcidrpvkg  ) =======================================

In this thematic  conversation on S-curves, I am in conversation with my colleague and Coach at PM Power, Anantha Natarajan. In this conversation, Anand, as he prefers to be called, shared various significant S-curves in his personal and professional life includingDecision to enter the software industry,Migrating to Australia, Pursuing an MBA, and Transitioning to a leadership role. He emphasized the importance of considering multiple dimensions beyond career goals, such as personal growth, family relationships, and financial stability.

In this podcast episode, we explore one of the most crucial tools for a successful eCommerce experience: your store's search function. Joining us is Arv Natarajan, Director of Product at GroupBy Inc. Arv shares his insights on improving search capabilities to enhance customer satisfaction and conversion rates. We discuss data catalog quality, the role of AI in search engines, and how to optimize merchandising with analytics. Tune in to learn how to boost your online store's performance with smarter search tools!Topics discussed in this episode:  Why improving search quality is crucial for ecommerce successHow product data quality impacts search performanceWhat advanced search capabilities like natural language processing can offerWhy analytics and understanding user search behavior is importantHow to balance AI-powered search with human curation and merchandisingWhat types of ecommerce businesses benefit most from advanced searchHow the search solution integrates with custom ecommerce themesWhat the future of AI-powered ecommerce search and product discovery might look likeLinks & ResourcesWebsite: https://www.groupbyinc.com/integrations/shopifyShopify App Store: https://apps.shopify.com/groupby-ai-search-discoveryLinkedIn: https://www.linkedin.com/in/arvnatarajan/X/Twitter: https://x.com/groupbyincGet access to more free resources by visiting the show notes athttps://t.ly/GECxQSign up for our free newsletter. Become a smarter online seller in just 10 minutes per week. The Ecommerce Coffee Break keeps ecommerce professionals updated with curated industry news, DTC insights, latest trends, and actionable advice. Perfect for anyone who wants to stay informed but is short on time. 100% free. Delivered every Thursday to your inbox. No Spam. Unsubscribe anytime. Sign up at https://newsletter.ecommercecoffeebreak.com Rate, Review & Follow on Apple Podcasts Enjoying this episode? Help others like you by rating and reviewing my show on Apple Podcasts! Your feedback supports more people in achieving their online business dreams. Click below, give five stars, and share your favorite part in a review! Click here: https://podcasts.apple.com/us/podcast/ecommerce-coffee-break-digital-marketing-podcast-for/id1567749422And if you haven't yet, follow the podcast to catch all the bonus episodes I'm adding. Don't miss out—hit that follow button now!

Pradeep is a brilliant geneticist and Director of Preventive Cardiology, holds the Paul & Phyllis Fireman Endowed Chair in Vascular Medicine at Mass General Hospital and on faculty at Harvard Medical School and the Broad Institute. His prolific research has been illuminating for the field of improving our approach to reduce the risk of heart disease. That's especially important because heart disease is the global (and US) #1 killer and is on the increase. We didn't get into lifestyle factors here since there was so much ground to cover on new tests. drugs, and strategies.A video snippet of our conversation on ApoB. Full videos of all Ground Truths podcasts can be seen on YouTube here. The audios are also available on Apple and Spotify.Transcript with links to key publications and audioEric Topol (00:06):Well, welcome to Ground Truths. I'm Eric Topol and with me is Pradeep Natarajan from Harvard. He's Director of Preventative Cardiology at the Mass General Brigham Health System and he has been lighting it up on the field of cardiovascular. We're going to get to lots of different parts of that story and so, Pradeep welcome.Pradeep Natarajan (00:31):Thanks Eric, really delighted and honored to be with you and have this discussion.Eric Topol (00:36):Well, for years I've been admiring your work and it's just accelerating and so there's so many things to get to. I thought maybe what we'd start off with is you recently wrote a New England Journal piece about two trials, two different drugs that could change the landscape of cardiovascular prevention in the future. I mean, that's one of the themes we're going to get to today is all these different markers and drugs that will change cardiology as we know it now. So maybe you could just give us a skinny on that New England Journal piece.Two New Lipid Targets With RNA DrugsPradeep Natarajan (01:16):Yeah, yeah, so these two agents, the trials were published at the same time. These phase two clinical trials for plozasiran, which is an siRNA against APOC3 and zodasiran, which is an siRNA against ANGPTL3. The reason why we have medicines against those targets are based on human genetics observations, that individuals with loss of function mutations and either of those genes have reduced lipids. For APOC3, it's reduced triglycerides for ANGPTL3 reduced LDL cholesterol and reduced triglycerides and also individuals that have those loss of function mutations also have lower risk for coronary artery disease. Now that's a very similar parallel to PCSK9. We have successful medicines that treat that target because people have found that carriers of loss of function mutations in PCSK9 lead to lower LDL cholesterol and lower coronary artery disease.(02:11):Now that suggests that therapeutic manipulation without significant side effects from the agents themselves for APOC3 and ANGPTL3 would be anticipated to also lower coronary artery disease risk potentially in complementary pathways to PCSK9. The interesting thing with those observations is that they all came from rare loss of function mutations that are enriched in populations of individuals. However, at least for PCSK9, has been demonstrated to have efficacy in large groups of individuals across different communities. So the theme of that piece was really just the need to study diverse populations because those insights are not always predictable about which communities are going to have those loss of function mutations and when you find them, they often have profound insights across much larger groups of individuals.Eric Topol (03:02):Well, there's a lot there that we can unpack a bit of it. One of them is the use of small interfering RNAs (siRNA) as drugs. We saw in the field of PCSK9, as you mentioned. First there were monoclonal antibodies directed against this target and then more recently, there's inclisiran which isn't an RNA play if you will, where you only have to take it twice a year and supposedly it's less expensive and I'm still having trouble in my practice getting patients covered on their insurance even though it's cheaper and much more convenient. But nonetheless, now we're seeing these RNA drugs and maybe you could comment about that part and then also the surprise that perhaps is unexplained is the glucose elevation.Pradeep Natarajan (03:53):Yeah, so for medicines and targets that have been discovered through human genetics, those I think are attractive for genetic-based therapies and longer interval dosing for the therapies, which is what siRNAs allow you to do because the individuals that have these perturbations, basically the naturally occurring loss of function mutations, they have these lifelong, so basically have had a one-time therapy and have lived, and so far, at least for these targets, have not had untoward side effects or untoward phenotypic consequences and only reduce lipids and reduce coronary artery disease. And so, instead of taking a pill daily, if we have conviction that that long amount of suppression may be beneficial, then longer interval dosing and not worrying about the pill burden is very attractive specifically for those specific therapeutics. And as you know, people continue to innovate on further prolonging as it relates to PCSK9.(04:57):Separately, some folks are also developing pills because many people do feel that there's still a market and comfort for daily pills. Now interestingly for the siRNA for zodasiran at the highest dose, actually for both of them at the highest doses, but particularly for zodasiran, there was an increase in insulin resistance parameters actually as it relates to hyperglycemia and less so as it relates to insulin resistance, that is not predicted based on the human genetics. Individuals with loss of function mutations do not have increased risks in hyperglycemia or type 2 diabetes, so that isolates it related to that specific platform or that specific technology. Now inclisiran, as you'd mentioned, Eric is out there. That's an siRNA against PCSK9 that's made by a different manufacturer. So far, the clinical trials have not shown hyperglycemia or type 2 diabetes as it relates inclisiran, so it may be related to the specific siRNAs that are used for those targets. That does merit further consideration. Now, the doses that the manufacturers do plan to use in the phase three clinical trials are at lower doses where there was not an increase in hyperglycemia, but that does merit further investigation to really understand why that's the case. Is that an expected generalized effect for siRNAs? Is it related to siRNAs for this specific target or is it just related to the platform used for these two agents which are made by the same manufacturer?Eric Topol (06:27):Right, and I think the fact that it's a mystery is intriguing at the least, and it may not come up at the doses that are used in the trials, but the fact that it did crop up at high doses is unexpected. Now that is part of a much bigger story is that up until now our armamentarium has been statins and ezetimibe to treat lipids, but it's rapidly expanding Lp(a), which for decades as a cardiologist we had nothing to offer. There may even be drugs to be able to lower people who are at high risk with high Lp(a). Maybe you could discuss that.What About Lp(a)?Pradeep Natarajan (07:13):Yeah, I mean, Eric, as you know, Lp(a) has been described as a cardiovascular disease risk factors for quite so many years and there are assays to detect lipoprotein(a) elevation and have been in widespread clinical practice increasing widespread clinical practice, but we don't yet have approved therapies. However, there is an abundance of literature preclinical data that suggests that it likely is a causal factor, meaning that if you lower lipoprotein(a) when elevated, you would reduce the risk related to lipoprotein(a). And a lot of this comes from similar human genetic studies. The major challenge of just relating a biomarker to an outcome is there are many different reasons why a biomarker might be elevated, and so if you detect a signal that correlates a biomarker, a concentration to a clinical outcome, it could be related to that biomarker, but it could be to the other reasons that the biomarker is elevated and sometimes it relates to the outcome itself.(08:10):Now human genetics is very attractive because if you find alleles that strongly relate to that exposure, you can test those alleles themselves with the clinical outcome. Now the allele assignment is established at birth. No other factor is going to change that assignment after conception, and so that provides a robust, strong causal test for that potential exposure in clinical outcome. Now, lipoprotein(a) is unique in that it is highly heritable and so there are lots of different alleles that relate to lipoprotein(a) and so in a well powered analysis can actually test the lipoprotein(a) SNPs with the clinical outcomes and similar to how there is a biomarker association with incident myocardial infarction and incident stroke, the SNPs related to lipoprotein(a) show the same. That is among the evidence that strongly supports that this might be causal. Now, fast forward to many years later, we have at least three phase three randomized clinical trials testing agents that have been shown to be very potent at lowering lipoprotein(a) that in the coming years we will know if that hypothesis is true. Importantly, we will have to understand what are the potential side effects of these medicines. There are antisense oligonucleotides and siRNAs that are primarily in investigation. Again, this is an example where there's a strong genetic observation, and so these genetic based longer interval dosing therapies may be attractive, but side effects will be a key thing as well too. Those things hard to anticipate really can anticipate based on the human genetics for off target effects, for example.(09:52):It's clearly a risk signal and hopefully in the near future we're going to have specific therapies.Eric Topol (09:57):Yeah, you did a great job of explaining Mendelian randomization and the fact the power of genetics, which we're going to get into deeper shortly, but the other point is that do you expect now that there's these multiple drugs that lower Lp(a) efficiently, would that be enough to get approval or will it have to be trials to demonstrate improved cardiovascular outcomes?Pradeep Natarajan (10:24):There is a great regulatory path at FDA for approval just for LDL cholesterol lowering and inclisiran is on the market and the phase three outcomes data has not yet been reported because there is a wide appreciation that LDL cholesterol lowering is a pretty good surrogate for cardiovascular disease risk lowering. The label will be restricted to LDL cholesterol lowering and then if demonstrated to have clinical outcomes, the label could be expanded. For other biomarkers including lipoprotein(a), even though we have strong conviction that it is likely a causal factor there hasn't met the bar yet to get approval just based on lipoprotein(a) lowering, and so we would need to see the outcomes effects and then we would also need to understand side effects. There is a body of literature of side effects for other therapies that have targeted using antisense oligonucleotides. We talked about potential side effects from some siRNA platforms and sometimes those effects could overtake potential benefits, so that really needs to be assessed and there is a literature and other examples.(11:31):The other thing I do want to note related to lipoprotein(a) is that the human genetics are modeled based on lifelong perturbations, really hard to understand what the effects are, how great of an effect there might be in different contexts, particularly when introduced in middle age. There's a lot of discussion about how high lipoprotein(a) should be to deliver these therapies because the conventional teaching is that one in five individuals has high lipoprotein(a), and that's basically greater than 75 nanomoles per liter. However, some studies some human genetic studies to say if you want to get an effect that is similar to the LDL cholesterol lowering medicines on the market, you need to start with actually higher lipoprotein(a) because you need larger amounts of lipoprotein(a) lowering. Those are studies and approaches that haven't been well validated. We don't know if that's a valid approach because that's modeling based on this sort of lifelong effect. So I'm very curious to see what the overall effect will be because to get approval, I think you need to demonstrate safety and efficacy, but most importantly, these manufacturers and we as clinicians are trying to find viable therapies in the market that it won't be hard for us to get approval because hopefully the clinical trial will have said this is the context where it works. It works really well and it works really well on top of the existing therapies, so there are multiple hurdles to actually getting it directly to our patients.How Low Do You Go with LDL Cholesterol?Eric Topol (13:02):Yeah, no question about that. I'm glad you've emphasized that. Just as you've emphasized the incredible lessons from the genetics of people that have helped guide this renaissance to better drugs to prevent cardiovascular disease. LDL, which is perhaps the most impressive surrogate in medicine, a lab test that you already touched on, one of the biggest questions is how low do you go? That is Eugene Braunwald, who we all know and love. They're in Boston. The last time I got together with him, he was getting his LDL down to close to zero with various tactics that might be extreme. But before we leave these markers, you're running preventive cardiology at man's greatest hospital. Could you tell us what is your recipe for how aggressive do you go with LDL?Pradeep Natarajan (14:04):Yeah, so when I talk to patients where we're newly getting lipid lowering therapies on, especially because many people don't have a readout of abnormal LDL cholesterol when we're prescribing these medicines, it's just giving them a sense of what we think an optimal LDL cholesterol might be. And a lot of this is based on just empirical observations. So one, the average LDL cholesterol in the modern human is about 100 to 110 mg/dL. However, if you look at contemporary hunter gatherers and non-human primates, their average LDL is about 40 to 50 and newborn babies have an LDL cholesterol of about 30. And the reason why people keep making LDL cholesterol lowering medicines because as you stack on therapies, cardiovascular disease events continue to reduce including down to these very low LDL cholesterol values. So the population mean for LDL cholesterol is high and everybody likely has hypercholesterolemia, and that's because over the last 10,000 years how we live our lives is so dramatically different and there has not been substantial evolution over that time to change many of these features related to metabolism.(15:16):And so, to achieve those really low LDL cholesterol values in today's society is almost impossible without pharmacotherapies. You could say, okay, maybe everybody should be on pharmacotherapies, and I think if you did that, you probably would reduce a lot of events. You'll also be treating a lot of individuals who likely would not get events. Cardiovascular disease is the leading killer, but there are many things that people suffer from and most of the times it still is not cardiovascular disease. So our practice is still rooted in better identifying the individuals who are at risk for cardiovascular disease. And so, far we target our therapies primarily in those who have already developed cardiovascular disease. Maybe we'll talk about better identifying those at risk, but for those individuals it makes lots of sense to get it as low as possible. And the field has continued to move to lower targets.(16:07):One, because we've all recognized, at least based on these empirical observations that lower is better. But now increasingly we have a lot of therapies to actually get there, and my hope is that with more and more options and the market forces that influence that the cost perspective will make sense as we continue to develop more. As an aside, related aside is if you look at the last cholesterol guidelines, this is 2018 in the US this is the first time PCSK9 inhibitors were introduced in the guidelines and all throughout that there was discussions of cost. There are a lot of concerns from the field that PCSK9 inhibitors would bankrupt the system because so many people were on statins. And you look at the prior one that was in 2013 and cost was mentioned once it's just the cost effectiveness of statins. So I think the field has that overall concern.(17:01):However, over time we've gotten comfortable with lower targets, there are more medicines and I think some of this competition hopefully will drive down some of the costs, but also the overall appreciation of the science related to LDL. So long-winded way of saying this is kind of the things that we discussed just to give reassurance that we can go to low LDL cholesterol values and that it's safe and then we think also very effective. Nobody knows what the lower limit is, whether zero is appropriate or not. We know that glucose can get too low. We know that blood pressure can be too low. We don't know yet that limit for LDL cholesterol. I mean increasingly with these trials we'll see it going down really low and then we'll better appreciate and understand, so we'll see 40 is probably the right range.Eric Topol (17:49):40, you said? Yeah, okay, I'll buy that. Of course, the other thing that we do know is that if you push to the highest dose statins to get there, you might in some people start to see the hyperglycemia issue, which is still not fully understood and whether that is, I mean it's not desirable, but whether or not it is an issue, I guess it's still out there dangling. Now the other thing that since we're on LDL, we covered Lp(a), PCSK9, the siRNA, is ApoB. Do you measure ApoB in all your patients? Should that be the norm?Measuring ApoBPradeep Natarajan (18:32):Yeah, so ApoB is another blood test. In the standard lipid panel, you get four things. What's measured is cholesterol and triglycerides, they're the lipids insoluble in blood to get to the different tissues that get packaged in lipoprotein molecules which will have the cholesterol, triglycerides and some other lipids and proteins. And so, they all have different names as you know, right? Low density lipoprotein, high density lipoprotein and some others. But also in the lipid panel you get the HDL cholesterol, the amount of cholesterol in an HDL particle, and then most labs will calculate LDL cholesterol and LDL cholesterol has a nice relationship with cardiovascular disease. You lower it with statins and others. Lower risk for cardiovascular disease, turns out a unifying feature of all of these atherogenic lipoproteins, all these lipoproteins that are measured and unmeasured that relate to cardiovascular disease, including lipoprotein(a), they all have an additional protein called ApoB. And ApoB, at least as it relates to LDL is a pretty good surrogate of the number of LDL particles.(19:37):Turns out that that is a bit better at the population level at predicting cardiovascular disease beyond LDL cholesterol itself. And where it can be particularly helpful is that there are some patients out there that have an unexpected ratio between ApoB and LDL. In general, the ratio between LDL cholesterol and ApoB is about 1.1 and most people will have that rough ratio. I verify that that is the expected, and then if that is the expected, then really there is no role to follow ApoB. However, primarily the patients that have features related to insulin resistance have obesity. They may often have adequate looking LDL cholesterols, but their ApoB is higher. They have more circulating LDL particles relative to the total amount of LDL cholesterol, so smaller particles themselves. However, the total number of particles may actually be too high for them.(20:34):And so, even if the LDL cholesterol is at target, if the ApoB is higher, then you need to reduce. So usually the times that I just kind of verify that I'm at appropriate target is I check the LDL cholesterol, if that looks good, verify with the ApoB because of this ratio, the ApoB target should be about 10% lower. So if we're aiming for about 40, that's like 36, so relatively similar, and if it's there, I'm good. If it's not and it's higher, then obviously increase the LDL cholesterol lowering medicines because lower the ApoB and then follow the ApoB with the lipids going forward. The European Society of Cardiology has more emphasis on measuring ApoB, that is not as strong in the US guidelines, but there are many folks in the field, preventive cardiologists and others that are advocating for the increasing use of ApoB because I think there are many folks that are not getting to the appropriate targets because we are not measuring ApoB.Why Aren't We Measuring and Treating Inflammation?Eric Topol (21:37):Yeah, I think you reviewed it so well. The problem here is it could be part of the standard lipid panel, it would make this easy, but what you've done is a prudent way of selecting out people who it becomes more important to measure and moderate subsequently. Now this gets us to the fact that we're lipid centric and we don't pay homage to inflammation. So I wrote a recent Substack on the big miss on inflammation, and here you get into things like the monoclonal antibody to interleukin-6, the trial that CANTOS that showed significant reduction in cardiovascular events and fatal cancers by the way. And then you get into these colchicine trials two pretty good size randomized trials, and here the entry was coronary disease with a high C-reactive protein. Now somehow or other we abandon measuring CRP or other inflammatory markers, and both of us have had patients who have low LDLs but have heart attacks or significant coronary disease. So why don't we embrace inflammation? Why don't we measure it? Why don't we have better markers? Why is this just sitting there where we could do so much better? Even agents that are basically cost pennies like colchicine at low doses, not having to use a proprietary version could be helpful. What are your thoughts about us upgrading our prevention with inflammation markers?Pradeep Natarajan (23:22):Yeah, I mean, Eric, there is an urgent need to address these other pathways. I say urgent need because heart disease has the dubious distinction of being the leading killer in the US and then over the last 20 years, the leading killer in the world as it takes over non-communicable diseases. And really since the early 1900s, there has been a focus on developing pharmacotherapies and approaches to address the traditional modifiable cardiovascular disease risk factors. That has done tremendous good, but still the curves are largely flattening out. But in the US and in many parts of the world, the deaths attributable to cardiovascular disease are starting to tick up, and that means there are many additional pathways, many of them that we have well recognized including inflammation. More recently, Lp(a) that are likely important for cardiovascular disease, for inflammation, as you have highlighted, has been validated in randomized controlled trials.(24:18):Really the key trial that has been more most specific is one on Canakinumab in the CANTOS trial IL-1β monoclonal antibody secondary prevention, so cardiovascular disease plus high C-reactive protein, about a 15% reduction in cardiovascular disease and also improvement in cancer related outcomes. Major issues, a couple of issues. One was increased risk for severe infections, and the other one is almost pragmatic or practical is that that medicine was on the market at a very high price point for rare autoinflammatory conditions. It still is. And so, to have for a broader indication like cardiovascular disease prevention would not make sense at that price point. And the manufacturer tried to go to the FDA and focus on the group that only had C-reactive protein lowering, but that's obviously like a backwards endpoint. How would you know that before you release the medicine? So that never made it to a broader indication.(25:14):However, that stuck a flag in the broader validation of that specific pathway in cardiovascular disease. That pathway has direct relevance to C-reactive protein. C-reactive protein is kind of a readout of that pathway that starts from the NLRP3 inflammasome, which then activates IL-1β and IL-6. C-reactive protein we think is just a non causal readout, but is a reliable test of many of these features and that's debatable. There may be other things like measuring IL-6, for example. So given that there is actually substantial ongoing drug development in that pathway, there are a handful of companies with NLRP3 inflammasome inhibitors, but small molecules that you can take as pills. There is a monoclonal antibody against IL-6 that's in development ziltivekimab that's directed at patients with chronic kidney disease who have lots of cardiovascular disease events despite addressing modifiable risk factors where inflammatory markers are through the roof.(26:16):But then you would also highlighted one anti-inflammatory that's out there that's pennies on the dollar, that's colchicine. Colchicine is believed to influence cardiovascular disease by inhibiting NLRP3, I say believed to. It does a lot of things. It is an old medicine, but empirically has been shown in at least two randomized controlled trials patients with coronary artery disease, actually they didn't measure C-reactive protein in the inclusion for these, but in those populations we did reduce major adverse cardiovascular disease events. The one thing that does give me pause with colchicine is that there is this odd signal for increased non-cardiovascular death. Nobody understands if that's real, if that's a fluke. The FDA just approved last year low dose colchicine, colchicine at 0.5 milligrams for secondary prevention given the overwhelming efficacy. Hasn't yet made it into prevention guidelines, but I think that's one part that does give me a little bit pause. I do really think about it particularly for patients who have had recurrent events. The people who market the medicine and do research do remind us that C-reactive protein was not required in the inclusion, but nobody has done that secondary assessment to see if measuring C-reactive protein would be helpful in identifying the beneficial patients. But I think there still could be more work done on better identifying who would benefit from colchicine because it's an available and cheap medicine. But I'm excited that there is a lot of development in this inflammation area.Eric Topol (27:48):Yeah, well, the development sounds great. It's probably some years away. Do you use colchicine in your practice?Pradeep Natarajan (27:56):I do. Again, for those folks who have had recurrent events, even though C-reactive protein isn't there, it does make me feel like I'm treating inflammation. If C-reactive protein is elevated and then I use it for those patients, if it's not elevated, it's a much harder sell from my standpoint, from the patient standpoint. At the lower dose for colchicine, people generally are okay as far as side effects. The manufacturer has it at 0.5 milligrams, which is technically not pennies on the dollar. That's not generic. The 0.6 milligrams is generic and they claim that there is less side effects at the 0.5 milligrams. So technically 0.6 milligrams is off label. So it is what it is.CHIP and Defining High Risk People for CV DiseaseEric Topol (28:40):It's a lot more practical, that's for sure. Now, before I leave that, I just want to mention when I reviewed the IL-1β trial, you mentioned the CANTOS trial and also the colchicine data. The numbers of absolute increases for infection with the antibody or the cancers with the colchicine are really small. So I mean the benefit was overriding, but I certainly agree with your concern that there's some things we don't understand there that need to be probed more. Now, one of the other themes, well before one other marker that before we get to polygenic risk scores, which is center stage here, defining high risk people. We've talked a lot about the conventional things and some of the newer ways, but you've been one of the leaders of study of clonal hematopoiesis of indeterminate potential known as CHIP. CHIP, not the chips set in your computer, but CHIP. And basically this is stem cell mutations that increase in people as we age and become exceptionally common with different mutations that account in these clones. So maybe you can tell us about CHIP and what I don't understand is that it has tremendous correlation association with cardiovascular outcomes adverse as well as other system outcomes, and we don't measure it and we could measure it. So please take us through what the hell is wrong there.Pradeep Natarajan (30:14):Yeah, I mean this is really exciting. I mean I'm a little bit biased, but this is observations that have been made only really over the last decade, but accelerating research. And this has been enabled by advances in genomic technologies. So about 10 years or plus ago, really getting into the early days of population-based next generation sequencing, primarily whole exome sequencing. And most of the DNA that we collect to do these population-based analyses come from the blood, red blood cells are anucleate, so they're coming from white blood cells. And so, at that time, primarily interrogating what is the germline genetic basis for coronary artery disease and early onset myocardial infarction. At the same time, colleagues at the Broad Institute were noticing that there are many additional features that you can get from the blood-based DNA that was being processed by the whole exome data. And there were actually three different groups that converged on that all in Boston that converged on the same observation that many well-established cancer causing mutations.(31:19):So mutations that are observed in cancers that have been described to drive the cancers themselves were being observed in these large population-based data sets that we were all generating to understand the relationship between loss of function mutations in cardiovascular disease. That's basically the intention of those data sets for being generated for other things. Strong correlation with age, but it was very common among individuals greater than 70; 10% of them would have these mutations and is very common because blood cancer is extremely, it's still pretty rare in the population. So to say 10% of people had cancer causing driver mutations but didn't have cancer, was much higher than anyone would've otherwise expected. In 2014, there were basically three main papers that described that, and they also observed that there is a greater risk of death. You'd say, okay, this is a precancerous lesion, so they're probably dying of cancer.(32:17):But as I said, the absolute incidence rate for blood cancer is really low and there's a relative increase for about tenfold, but pretty small as it relates to what could be related to death. And in one of the studies we did some exploratory analysis that suggested maybe it's actually the most common cause of death and that was cardiovascular disease. And so, a few years later we published a study that really in depth really looked at a bunch of different data sets that were ascertained to really understand the relationship between these mutations, these cancer causing mutations in cardiovascular disease, so observed it in enrichment and older individuals that had these mutations, CHIP mutations, younger individuals who had early onset MI as well too, and then also look prospectively and showed that it related to incident coronary artery disease. Now the major challenge for this kind of analysis as it relates to the germline genetic analysis is prevalence changes over time.(33:15):There are many things that could influence the presence of clonal hematopoiesis. Age is a key enriching factor and age is the best predictor for cardiovascular disease. So really important. So then we modeled it in mice. It was actually a parallel effort at Boston University (BU) that was doing the same thing really based on the 2014 studies. And so, at the same time we also observed when you modeled this in mice, you basically perturb introduce loss of function mutations in the bone marrow for these mice to recapitulate these driver mutations and those mice also have a greater burden of atherosclerosis. And Eric, you highlighted inflammation because basically the phenotype of these cells are hyper inflamed cells. Interestingly, C-reactive protein is only modestly elevated. So C-reactive protein is not fully capturing this, but many of the cytokines IL-1β, IL-6, they're all upregulated in mice and in humans when measured as well.(34:11):Now there've been a few key studies that have been really exciting about using anti-inflammatories in this pathway to address CHIP associated cardiovascular disease. So one that effort that I said in BU because they saw these cytokines increased, we already know that these cytokines have relationship with atherosclerosis. So they gave an NLRP3 inflammasome inhibitor to the mice and they showed that the mice with or without CHIP had a reduction in atherosclerosis, but there was a substantial delta among the mice that are modeled as having CHIP. Now, the investigators in CANTOS, the manufacturers, they actually went back and they survey where they had DNA in the CANTOS trial. They measured CHIP and particularly TET2 CHIP, which is the one that has the strongest signal for atherosclerosis. As I said, overall about 15% reduction in the primary outcome in CANTOS. Among the individuals who had TET2 CHIP, it was a 64% reduction in event.(35:08):I mean you don't see those in atherosclerosis related trials. Now this has the caveat of it being secondary post hoc exploratory, the two levels of evidence. And so, then we took a Mendelian randomization approach. Serendipitously, just so happens there is a coding mutation in the IL-6 receptor, a missense mutation that in 2012 was described that if you had this mutation, about 40% of people have it, you have a 5%, but statistically significant reduction in coronary artery disease. So we very simply said, if the pathway of this NLRP3 inflammasome, which includes IL-6, if you have decreased signaling in that pathway, might you have an even greater benefit from having that mutation if you had CHIP versus those who didn't have CHIP. So we looked in the UK Biobank, those who didn't have CHIP 5% reduction, who had that IL-6 receptor mutation, and then those who did have CHIP, if they had that mutation, it was about a 60% reduction in cardiovascular disease.(36:12):Again, three different lines of evidence that really show that this pathway has relevance in the general population, but the people who actually might benefit the most are those with CHIP. And I think as we get more and more data sets, we find that not all of the CHIP mutations are the same as it relates to cardiovascular disease risk. It does hone in on these key subsets like TET2 and JAK2, but this is pretty cool as a preventive cardiologist, new potential modifiable risk factor, but now it's almost like an oncologic paradigm that is being applied to coronary artery disease where we have specific driver mutations and then we're tailoring our therapies to those specific biological drivers for coronary artery disease. Hopefully, I did that justice. There's a lot there.Why Don't We Measure CHIP?Eric Topol (36:57):Well, actually, it's phenomenal how you've explained that, but I do want to review for our listeners or readers that prior to this point in our conversation, we were talking about germline mutations, the ones you're born with. With CHIP, we're talking about acquired somatic mutations, and these are our blood stem cells. And what is befuddling to me is that with all the data that you and others, you especially have been publishing and how easy it would be to measure this. I mean, we've seen that you can get it from sequencing no less other means. Why we don't measure this? I mean, why are we turning a blind eye to CHIP? I just don't get it. And we keep calling it of indeterminate potential, not indeterminate. It's definite potential.Pradeep Natarajan (37:51):Yeah, no, I think these are just overly cautious terms from the scientists. Lots of people have CHIP, a lot of people don't have clinical outcomes. And so, I think from the lens of a practicing hematologists that provide some reassurance on the spectrum for acquired mutation all the way over to leukemia, that is where it comes from. I don't love the acronym as well because every subfield in biomedicine has its own CHIP, so there's obviously lots of confusion there. CH or clinical hematopoiesis is often what I go, but I think continuing to be specific on these mutations. Now the question is why measure? Why aren't we measuring it? So there are some clinical assays out there. Now when patients get evaluated for cytopenias [low cell counts], there are next generation sequencing tests that look for these mutations in the process for evaluation. Now, technically by definition, CHIP means the presence of these driver mutations that have expanded because it's detectable by these assays, not a one-off cell because it can only be detected if it's in a number of cells.(38:55):So there has been some expansion, but there are no CBC abnormalities. Now, if there's a CBC abnormality and you see a CHIP mutation that's technically considered CCUS or clonal cytopenia of unknown significance, sometimes what is detected is myelodysplastic syndrome. In those scenarios still there is a cardiovascular disease signal, and so many of our patients who are seen in the cancer center who are being evaluated for these CBC abnormalities will be detected to have these mutations. They will have undergone some risk stratification to see what the malignancy potential is. Still pretty low for many of those individuals. And so, the major driver of health outcomes for this finding may be cardiovascular. So those patients then get referred to our program. Dana-Farber also has a similar program, and then my colleague Peter Libby at the Brigham often sees those patients as well. Now for prospective screening, so far, an insurance basically is who's going to pay for it.(39:51):So an insurance provider is not deemed that appropriate yet. You do need the prospective clinical trials because the medicines that we're talking about may have side effects as well too. And what is the yield? What is the diagnostic yield? Will there actually be a large effect estimate? But there has been more and more innovation, at least on the assay and the cost part of the assay because these initial studies, we've been using whole exome sequencing, which is continuing to come down, but is not a widely routine clinical test yet. And also because as you highlighted, these are acquired mutations. A single test is not necessarily one and done. This may be something that does require surveillance for particular high risk individuals. And we've described some risk factors for the prevalence of CHIP. So surveillance may be required, but because there are about 10 genes that are primarily implicated in CHIP, that can substantially decrease the cost of it. The cost for DNA extraction is going down, and so there are research tests that are kind of in the $10 to $20 range right now for CHIP. And if flipped over to the clinical side will also be reasonably low cost. And so, for the paradigm for clinical implementation, that cost part is necessary.Eric Topol (41:10):I don't know the $10 or $20 ones. Are there any I could order on patients that I'm worried about?Pradeep Natarajan (41:17):Not yet clinical. However, there is a company that makes the reagents for at least the cores that are developing this. They are commercializing that test so that many other cores, research cores can develop it. I think it's in short order that clinical labs will adopt it as well too.Eric Topol (41:36):That's great.Pradeep Natarajan (41:37):I will keep you apprised.What About Polygenic Risk Scores?Eric Topol (41:39):I think that's really good news because like I said, we're so darn lipid centric and we have to start to respect the body of data, the knowledge that you and others have built about CHIP. Now speaking of another one that drives me nuts is polygenic risk score (PRS) for about a decade, I've been saying we have coronary disease for most people is a polygenic trait. It's not just a familial hypercholesterolemia. And we progressively have gotten better and better of the hundreds of single variants that collectively without a parental history will be and independently predict who is at double, triple or whatever risk of getting heart disease, whereby you could then guide your statins at higher aggressive or pick a statin, use one or even go beyond that as we've been talking about. But we don't use that in practice, which is just incredible because it's can be done cheap.(42:45):You can get it through whether it's 23andMe or now many other entities. We have an app, MyGeneRank where we can process that Scripss does for free. And only recently, Mass General was the first to implement that in your patient population, and I'm sure you were a driver of that. What is the reluctance about using this as an orthogonal, if you will, separate way to assess a person's risk for heart disease? And we know validated very solidly about being aggressive about lipid lowering when you know this person's in the highest 5% polygenic risk score. Are we just deadheads in this field or what?Pradeep Natarajan (43:30):Yeah, I mean Eric, as you know, lots of inertia in medicine, but this one I think has a potential to make a large impact. Like CHIP mutations, I said news is about 10% in individuals greater than 70. The prospect here is to identify the risk much earlier in life because I think there is a very good argument that we're undertreating high risk individuals early on because we don't know how to identify them. As you highlighted, Dr. Braunwald about LDL cholesterol. The other part of that paradigm is LDL cholesterol lowering and the duration. And as we said, everybody would benefit from really low LDL cholesterol, but again, you might overtreat that if you just give that to everybody. But if you can better identify the folks very early in life, there is a low cost, low risk therapy, at least related to statins that you could have a profound benefit from the ones who have a greater conviction will have future risk for cardiovascular disease.(44:21):You highlighted the family history, and the family history has given the field of clues that genetics play a role. But as the genome-wide association studies have gotten larger, the polygenic risk scores have gotten better. We know that family history is imperfect. There are many reasons why a family member who is at risk may or may not have developed cardiovascular disease. A polygenic risk score will give a single number that will estimate the contribution of genetics to cardiovascular disease. And the thing that is really fascinating to me, which is I think some of a clinical implementation challenge is that the alleles for an individual are fixed. The genotyping is very cheap. That continues to be extremely cheap to do this test. But the weights and the interpretation of what the effects should be for each of the SNPs are continually being refined over time.(45:18):And so, given the exact same SNPs in the population, the ability to better predict cardiovascular diseases getting better. And so, you have things that get reported in the literature, but literally three years later that gets outdated and those hypotheses need to be reassessed. Today, I'll say we have a great relative to other things, but we have a great polygenic risk score was just reported last year that if you compare it to familial hypercholesterolemia, which has a diagnostic yield of about 1 in 300 individuals, but readily detectable by severe hypercholesterolemia that has about threefold risk for cardiovascular disease. By polygenic risk score, you can find 1 in 5 individuals with that same risk. Obviously you go higher than that, it'll be even higher risk related to that. And that is noble information very early in life. And most people develop risk factors later in life. It is happening earlier, but generally not in the 30s, 40s where there's an opportunity to make a substantial impact on the curve related to cardiovascular disease.(46:25):But there is a lot of momentum there. Lots of interest from NIH and others. The major challenge is though the US healthcare system is really not well set up to prevention, as you know, we practice healthcare after patient's developed disease and prevent the complications related to progression. The stakeholder incentives beyond the patient themselves are less well aligned. We've talked a lot here today about payers, but we don't have a single payer healthcare system. And patients at different times of their lives will have different insurers. They'll start early in life with their parents, their first employer, they'll move on to the next job and then ultimately Medicare. There's no entity beyond yourself that really cares about your longevity basically from the beginning and your overall wellness. That tension has been a major challenge in just driving the incentives and the push towards polygenic risk scores. But there are some innovative approaches like MassMutual Life Insurance actually did a pilot on polygenic risk scoring.(47:33):They're in the business of better understanding longevity. They get that this is important data. Major challenges, there are federal protections against non-discrimination in the workplace, health insurance, not necessarily life insurance. So I think that there are lots of things that have to be worked out. Everybody recognizes that this is important, but we really have to have all the incentives aligned for this to happen at a system-wide level in the US. So there's actually lots of investment in countries that have more nationalized healthcare systems, lots of development in clinical trials in the UK, for example. So it's possible that we in the US will not be the lead in that kind of evidence generation, but maybe we'll get there.The GLP-1 DrugsEric Topol (48:16):Yeah, it's frustrating though, Pradeep, because this has been incubating for some time and now we have multi ancestry, polygenic risk scores, particularly for heart disease and we're not using it, and it's not in my view, in the patient's best interest just because of these obstacles that you're mentioning, particularly here in the US. Well, the other thing I want to just get at with you today is the drugs that we were using for diabetes now blossoming for lots of other indications, particularly the glucagon-like peptide 1 (GLP-1) drugs. This has come onto the scene in recent years, not just obviously for obesity, but it's anti-inflammatory effects as we're learning, mediated not just through the brain but also T cells and having extraordinary impact in heart disease for people with obesity and also with those who have heart failure, about half of heart failure for preserved ejection fraction. So recently you and your colleagues recently published a paper with this signal of optic neuropathy. It was almost seven eightfold increase in a population. First, I wanted to get your sense about GLP-1. We're also going to get into the SGLT2 for a moment as well, but how do you use GLP-1? What's your prognosis for this drug class going forward?Pradeep Natarajan (49:55):As it relates to the paper, I can't claim credit as one of my former students who is now Mass Eye and Ear resident who participated, but we can talk about that. There's obviously some challenges for mining real world data, but this was related to anecdotes that they were observing at Mass Eye and Ear and then studied and observed an enrichment. In general though, I feel like every week I'm reading a new clinical trial about a new clinical outcome benefit as it relates to GLP-1 receptor agonists. This is kind of one thing that stands out that could be interrogated in these other clinical trials. So I would have that caveat before being cautious about ocular complications. But the data has been overwhelmingly beneficial, I think, because at minimum, obesity and inflammation are relayed to myriad of consequences, and I'm really excited that we have therapies that can address obesity that are safe.(50:52):There's a legacy of unsafe medicines for obesity, especially related to cardiovascular disease. So the fact that we have medicines that are safe and effective for lowering weight that also have real strong effects on clinical outcomes is tremendous. We in cardiology are increasingly using a range of diabetes medicines, including GLP-1 receptor agonists and SGLT2 inhibitors. I think that is also the secular changes of what influences cardiovascular disease over time. I talked about over the last 10 years or so with this increase in deaths attributable to cardiovascular disease. If you look at the influences of traditional clinical risk factors today, many of them have decreased in importance because when abnormal, we recognize them, in general we modify them when recognized. And so, many of the things that are unaddressed, especially the features related to insulin resistance, obesity, they start rising in importance. And so, there is a dramatic potential for these kinds of therapies in reducing the residual risks that we see related to cardiovascular disease. So I'm enthusiastic and excited. I think a lot more biology that needs to be understood of how much of this is being influenced specifically through this pathway versus a very effective weight loss medicine. But also interesting to see the insights on how the effect centrally on appetite suppression has profound influences on weight loss as well too. And hopefully that will lead to more innovations in weight management.The SGLT-2 DrugsEric Topol (52:25):And likewise, perhaps not getting near as much play, but when it came on the cardiovascular scene that an anti-diabetic drug SGLT2 was improving survival, that was big, and we still don't know why. I mean, there's some ideas that it might be a senolytic drug unknowingly, but this has become a big part of practice of cardiology in patients with diabetes or with preserved ejection fraction heart failure. Is that a fair summary for that drug?Pradeep Natarajan (53:00):Yeah, I totally agree. I mean, as there has been increased recognition for heart failure preserved ejection fraction, it has been almost disheartening over the last several years that we have not had very specific effective therapies to treat that condition. Now, it is a tremendous boon that we do have medicines interestingly focused on metabolism that are very helpful in that condition for heart failure with preserved ejection fraction. But there is still much more to be understood as far as that condition. I mean, the major challenge with heart failure, as you know, especially with heart failure preserved ejection fraction, it likely is a mix of a wide variety of different etiologies. So in parallel with developing effective therapies that get at some aspect is really understanding what are the individual drivers and then targeting those specific individual drivers. That requires a lot of unbiased discovery work and further profiling to be done. So lot more innovation, but relative to heart failure itself, it is not had widespread recognition as heart failure reduced ejection fraction. So much more to innovate on, for sure.Eric Topol (54:07):Right, right. Yeah, I am stunned by the recent progress in cardiovascular medicine. You have been center stage with a lot of it, and we've had a chance to review so much. And speaking of genetics, I wanted to just get a little insight because I recently came across the fact that your mother here at the City of Hope in Southern California is another famous researcher. And is that, I don't know what chromosome that is on regarding parental transmission of leading research. Maybe you can tell me about that.Pradeep Natarajan (54:41):Yeah, I mean, I guess it is a heritable trait when a parent has one profession that there is a higher likelihood that the offspring will have something similar. So both of my parents are PhDs, nonphysicians. There is a diabetes department at the City of Hope, so she's the chair of that department. So very active. We do overlap in some circles because she does investigate both vascular complications and renal complications. And then sometimes will ask my advice on some visualization. But she herself has just had a science translational medicine paper, for example, just a couple of months ago. So it's fun to talk about these things. To be honest, because my parents are researchers, I was not totally sure that I would be a researcher and kind of wanted to do something different in medicine. But many of my early observations and just how common cardiovascular disease is around me and in my community and wanting to do something useful is what got me specifically into cardiology.(55:45):But obviously there are numerous outstanding, important questions. And as I went through my career, really focused on more basic investigations of atherosclerosis and lipids. What got me excited sort of after my clinical training was the ability to ask many of these questions now in human populations with many new biological data sets, at least first centered on genetics. And the capabilities continue to expand, so now I teach first year Harvard medical students in their genetics curriculum. And when I talk to them just about my career arc, I do remind them they're all doing millions of things and they're exploring lots of things, but when they get to my shoes, the capabilities will be tremendously different. And so, I really advise them to take the different experiences, mainly in an exercise for asking questions, thoughtfully addressing questions, connecting it back to important clinical problems. And then once they start to understand that with a few different approaches, then they'll totally take off with what the opportunities are down the road.Eric Topol (56:51):No, it's great. I mean, how lucky somebody could be in the first year of med school with you as their teacher and model. Wow. Pradeep, we've really gone deep on this and it's been fun. I mean, if there's one person I'm going to talk to you about cardiovascular risk factors and the things that we've been into today, you would be the one. So thank you for taking the time and running through a lot of material here today, and all your work with great interest.Pradeep Natarajan (57:24):Thanks, Eric. I really appreciate it. It's tremendous honor. I'm a big fan, so I would be glad to talk about any of these things and more anytime.***************Thanks for listening, reading or watching!The Ground Truths newsletters and podcasts are all free, open-access, without ads.Please share this post/podcast with your friends and network if you found it informative!Voluntary paid subscriptions all go to support Scripps Research. Many thanks for that—they greatly helped fund our summer internship programs for 2023 and 2024.Thanks to my producer Jessica Nguyen and Sinjun Balabanoff for audio and video support at Scripps Research.Note: you can select preferences to receive emails about newsletters, podcasts, or all I don't want to bother you with an email for content that you're not interested in. Get full access to Ground Truths at erictopol.substack.com/subscribe

Sign Up to Receive Venkat's Weekly Newsletter Even as an engineer, Iswari found herself explaining concepts to her peers. Teaching gave her a purpose. She became a certified Montessori educator and later Director of a Montessori school.  Iswari believes it was that all-girls school she went to that built her self-confidence. Today as President of St. Mary's Academy, Iswari is helping her students build theirs. Iswari joins us on our podcast to share her professional background, journey from engineering to teaching, St. Mary's Academy Flagship Programs, All Girls School, AI Impact, and her Advice for High School students. In particular, we discuss the following with her:  Iswari Natarajan's Background St Mary's Academy - All Girls High School Flagship Programs Advice for High Schoolers Topics discussed in this episode: Introducing Iswari Natarajan, St. Mary's Academy [] Hi Fives - Podcast Highlights [] Professional Background  [] Engineering to Education [] The St Mary's Academy Opportunity [] Educator versus Engineer [] Flagship SMA Programs [] SMA Student Interests [] Experiential Learning [] Impact of AI [] All girls High School [] How Students are Handling 10X? [] Advice for High Schoolers [] Our Guest: Iswari Natarajan, President of St. Mary's Academy, Denver Colorado. Memorable Quote: “If you ever want to truly find joy, I always go and pretend I have an emergency in the kindergarten classroom. So that's where you can find joy. If you want to get sobered up and you want a reality check, that's Middle School, because they'll tell you, like what it is, and truly, if you want hope for the future, right? If you want to say what you know, like our world, no matter what's going on, is in good hands, you have to visit our high school.” Iswari Natarajan. Episode Transcript: Please visit Episode's Transcript. Recommended Episodes: College Experiences Calls-to-action: Follow us on Instagram. To Ask the Guest a question, or to comment on this episode, email podcast@almamatters.io. Subscribe or Follow our podcasts at any of these locations:Apple Podcasts, Spotify.

In this episode, host Shikha Jain, MD, speaks with Shyam Natarajan, PhD, about machine learning in cancer research and testing, using technological innovation to address disparities in health care trials and more. •    Welcome to another exciting episode of Oncology Overdrive 1:17 •    About Natarajan 1:22 •    The interview 2:10 •    How did you get into the medical technology space?  2:29 •    Can you explain what machine learning means?  4:37 •    How did you end up co-founding Avenda Health?  7:18 •    Do you think that this type of technology is replicable in other disease types as well? […] Where else do you see this being a benefit? 9:53 •    When you think about AI, what are the other applications for this type of technology outside of oncology?  11:24 •    How do you respond to concerns that AI is becoming too sentient or independent?  12:50 •    What are the checkpoints we need to put in place to make sure that biases in AI algorithms do not become the norm?  16:21 •    Do you have ways to predict who would benefit from these types of technology, and can you categorize patients into who is appropriate for trialing these technologies?  19:44 •    Is there a way to utilize this technology to address disparities in health care?  22:04 •    Have you found that there are specific things that make it harder to enroll patients in these particular clinical trials? How do you navigate those? 24:47 •    If you had a crystal ball that could see fifty years into the future, where do you see all of this technology going? 27:28 •    If someone could only listen to the last few minutes of this episode, what would you want them to take away? 30:56 •    How to contact Natarajan 31:31 •    Thanks for listening 32:22 Shyam Natarajan, PhD, is the co-founder and CEO of Avenda Health, a medtech company focused on improving outcomes for the one in seven men at risk for prostate cancer. We'd love to hear from you! Send your comments/questions to Dr. Jain at oncologyoverdrive@healio.com. Follow Healio on X and LinkedIn: @HemOncToday and https://www.linkedin.com/company/hemonctoday/. Follow Dr. Jain on X: @ShikhaJainMD. Natarajan can be reached at www.avendahealth.com or via LinkedIn.  Disclosures: Jain and Natarajan report no relevant financial disclosures. 

Today's guest is Prashant Natarajan, Vice President of Strategy and Products at H2O.ai. H2O.ai is a tech company whose platform, the H2O AI Cloud, enables businesses, government entities, nonprofits, and academic institutions to make, operate, and innovate with different AI capabilities like machine learning and AI-enhanced middleware. Prashant joins Emerj CEO and Head of Research Daniel Faggella on today's episode to discuss the impact generative AI is having on the healthcare industry and what leaders can do to drive adoption safely across the enterprise. To access Emerj's frameworks for AI readiness, ROI, and strategy, visit Emerj Plus at emerj.com/p1.

In this week's episode, we welcome back our first-ever guest on the pod. And it's safe to say we get through quite a lot. We discuss the influx of Koreans (and Russians) in Vietnam, job offers in Taiwan and more socio-economic policy chat which smarter people than us have almost certainly spent years studying, which we've butchered in less than a minute. We also get into being sent out of class in school/college, giving money to beggars in India and travellers “begpacking” around SE Asia. There's also bits and pieces about Mongolia, tipping culture in America and shooting cows with bazookas in Cambodia (not us). There really is something for eveyone in this one. Get on it.

In this final episode of her reminiscences, 90-year-old Mrs Jaya Natarajan takes us through a journey of heavenly visions and visits that not only bedazzled her but also healed her. In each of these episodes she saw the guiding and guarding hand of Bhagawan. In the 1990s, Swami sent her and her husband to middle-east. It was wartime there but Bhagawan appeared there to reassure her of His presence and protection, and later in 2010 gave her husband a new lease of life miraculously. This episode is full of such spectacular leelas that she has experienced firsthand.

91-year-old Mrs Jaya Natarajan continues with her spellbinding tales of divine miracles and interactions that she was fortunate to be part of in the sixties and seventies. In this fourth episode of her series, she recounts an amazing leela that unfolded when she decided to serve little children in the state of Madhya Pradesh as well as heartwarming moments of Divine grace she experienced during Bhagawan's visit to Delhi in 1978.

We often think that it is our spiritual aspirations, worldly needs or insurmountable problems that lead us to Bhagawan's fold. But, little do we realise that in reality, as Swami would say, it is the Lord who comes seeking those that belong to Him. Born into a family that wasn't given to regular forms of worship, and married into a household that was well-endowed but not particularly spiritual, 91-year-old devotee, Mrs Jaya Natarajan, in this second part of the conversation shares the inscrutable events, visions and encounters that were slowly preparing her for the grandest blessing of her life. The interview was recorded in 2023.

We often think that it is our spiritual aspirations, worldly needs or insurmountable problems that lead us to Bhagawan's fold. But, little do we realise that in reality, as Swami would say, it is the Lord who comes seeking those that belong to Him. Born into a family that wasn't given to regular forms of worship, and married into a household that was well-endowed but not particularly spiritual, 91-year-old devotee, Mrs Jaya Natarajan, in this first part of the conversation shares the inscrutable events, visions and encounters that were slowly preparing her for the grandest blessing of her life. The interview was recorded in 2023.

#SriSathyaSai #SaiBaba #PrasanthiNilayam #RadioSai #RadioSaiLive In this fifth episode of the reminiscences of Mrs Jaya Natarajan who was pulled to Bhagawan way back in the sixties, she narrates two revealing trips that Swami asked her to undertake to two hallowed sites. One was Shirdi and the other was to Jillellamudi, a sacred place in the Guntur district of Andhra Pradesh. In both these visits, the experiences Bhagawan conferred her with were truly incredible. So travel to two holy sites with this 90-year-old devotee of Bhagawan, who is herself a living miracle of His grace and love.

Dive into the future of medicine with Google researchers Khaled Saab and Vivek Natarajan, discussing the breakthroughs in AI for healthcare. Discover how AI doctors may soon provide high-quality medical advice, enhancing global access to healthcare. Learn about the innovative use of large language models in medical applications and the potential for AI to outperform human doctors. Listen as we explore the significance of AI's role in healthcare and its implications for future medical practices, featuring insights from leaders in AI research. SPONSORS: Oracle Cloud Infrastructure (OCI) is a single platform for your infrastructure, database, application development, and AI needs. OCI has four to eight times the bandwidth of other clouds; offers one consistent price, and nobody does data better than Oracle. If you want to do more and spend less, take a free test drive of OCI at https://oracle.com/cognitive The Brave search API can be used to assemble a data set to train your AI models and help with retrieval augmentation at the time of inference. All while remaining affordable with developer first pricing, integrating the Brave search API into your workflow translates to more ethical data sourcing and more human representative data sets. Try the Brave search API for free for up to 2000 queries per month at https://bit.ly/BraveTCR Omneky is an omnichannel creative generation platform that lets you launch hundreds of thousands of ad iterations that actually work customized across all platforms, with a click of a button. Omneky combines generative AI and real-time advertising data. Mention "Cog Rev" for 10% off https://www.omneky.com/ Head to Squad to access global engineering without the headache and at a fraction of the cost: head to https://choosesquad.com/ and mention “Turpentine” to skip the waitlist. RECOMMENDED PODCAST: Byrne Hobart, the writer of The Diff, is revered in Silicon Valley. You can get an hour with him each week. See for yourself how his thinking can upgrade yours. Spotify: https://open.spotify.com/show/6rANlV54GCARLgMOtpkzKt Apple: https://podcasts.apple.com/us/podcast/the-riff-with-byrne-hobart-and-erik-torenberg/id1716646486 CHAPTERS: (00:00:00) About the Show (00:04:34) Introduction (00:06:35) Flamingo (00:11:50) Importance of data quality (00:13:29) Amy: AI doctor (00:18:44) Simulation Learning Environment (00:23:26) Sponsors: Oracle | Brave (00:25:34) Training the Agents (00:27:29) Tens of thousands of data points (00:30:35) How to incorporate new knowledge (00:33:21) MedGemini (00:34:51) Sponsors: Omneky | Squad (00:36:38) Uncertainty guided search (00:39:29) Generalist models (00:41:16) MedGemini, Gemini, multimodal, medical images (00:44:57) Future work, integration, consolidation (00:46:00) Cost of AI (00:52:38) When will AI Doctors be Deployed? (00:58:22) The Speed of Trust (00:59:58) Societal Acceptance of AI Doctors (01:02:06) Uncertainty-Guided Search (01:06:02) Med-Gemini: Chest X-Rays and CT Scans (01:17:38) AI Scientist (01:20:01) What are the principles at play? (01:22:58) What should we do about AI? (01:28:24) LLM for democratizing access to care (01:34:22) Final Message (01:35:38) Closing (01:36:45) Outro

Community is the foundation on which success is built. A strong support network opens opportunities and helps us overcome even the most challenging adversity.On this episode, I'm joined by Prem Natarajan, Chief Scientist, EVP, and Head of Enterprise Data and AI at Capital One, to explore his journey from Chennai to leading AI initiatives at a major financial services company.Key Takeaways:(00:11) The value of continual security testing.(00:18) The importance of prioritizing your security issues.(19:47) How early life influences and role models shape career ambitions.(21:30) The critical role of mentors and asymmetrical mentorship relationships.(29:00) Learning life lessons through sports and teamwork.(36:22) Early technical projects shaping an engineering career.(41:00) Balancing foundational understanding with pragmatic goals in engineering.(50:23) The importance of curiosity and admitting when you don't know.(56:25) Transitioning from academia to industry and the AI revolution.(01:07:11) Family influence and persistence as a mantra.(01:08:51) Nurturing relationships and leveraging education.(01:09:13) Advice on leveraging education and imagination for young professionals.Resources Mentioned:Prem Natarajan - https://www.linkedin.com/in/natarajan/Capital One - https://www.linkedin.com/company/capital-one/BBN Technologies - https://www.bbn.com/University of Southern California - https://www.usc.edu/Amazon Alexa - https://developer.amazon.com/en-US/alexaThanks for listening to the Indianness podcast. If you enjoyed this episode, hit the subscribe button and never miss another insightful conversation with leaders of Indian origin. And be sure to leave a review to help get the word out about the show. #Indian #IndiaBusiness #India #Indianness

Episode 126I spoke with Vivek Natarajan about:* Improving access to medical knowledge with AI* How an LLM for medicine should behave* Aspects of training Med-PaLM and AMIE* How to facilitate appropriate amounts of trust in users of medical AI systemsVivek Natarajan is a Research Scientist at Google Health AI advancing biomedical AI to help scale world class healthcare to everyone. Vivek is particularly interested in building large language models and multimodal foundation models for biomedical applications and leads the Google Brain moonshot behind Med-PaLM, Google's flagship medical large language model. Med-PaLM has been featured in The Scientific American, The Economist, STAT News, CNBC, Forbes, New Scientist among others.I spend a lot of time on this podcast—if you like my work, you can support me on Patreon :)Reach me at editor@thegradient.pub for feedback, ideas, guest suggestions. Subscribe to The Gradient Podcast:  Apple Podcasts  | Spotify | Pocket Casts | RSSFollow The Gradient on TwitterOutline:* (00:00) Intro* (00:35) The concept of an “AI doctor”* (06:54) Accessibility to medical expertise* (10:31) Enabling doctors to do better/different work* (14:35) Med-PaLM* (15:30) Instruction tuning, desirable traits in LLMs for medicine* (23:41) Axes for evaluation of medical QA systems* (30:03) Medical LLMs and scientific consensus* (35:32) Demographic data and patient interventions* (40:14) Data contamination in Med-PaLM* (42:45) Grounded claims about capabilities* (45:48) Building trust* (50:54) Genetic Discovery enabled by a LLM* (51:33) Novel hypotheses in genetic discovery* (57:10) Levels of abstraction for hypotheses* (1:01:10) Directions for continued progress* (1:03:05) Conversational Diagnostic AI* (1:03:30) Objective Structures Clinical Examination as an evaluative framework* (1:09:08) Relative importance of different types of data* (1:13:52) Self-play — conversational dispositions and handling patients* (1:16:41) Chain of reasoning and information retention* (1:20:00) Performance in different areas of medical expertise* (1:22:35) Towards accurate differential diagnosis* (1:31:40) Feedback mechanisms and expertise, disagreement among clinicians* (1:35:26) Studying trust, user interfaces* (1:38:08) Self-trust in using medical AI models* (1:41:39) UI for medical AI systems* (1:43:50) Model reasoning in complex scenarios* (1:46:33) Prompting* (1:48:41) Future outlooks* (1:54:53) OutroLinks:* Vivek's Twitter and homepage* Papers* Towards Expert-Level Medical Question Answering with LLMs (2023)* LLMs encode clinical knowledge (2023)* Towards Generalist Biomedical AI (2024)* AMIE* Genetic Discovery enabled by a LLM (2023) Get full access to The Gradient at thegradientpub.substack.com/subscribe

Welcome to BrainX AI in Medicine Podcast series, where we bring in leaders within fields of AI and Medicine to discuss their cutting-edge research, explore boundaries of current knowledge, and provide insightful commentary on how to effectively lead the AI revolution in Medicine. Today's guest is Vivek Natarajan, who is a Research Scientist at Google leading research at the intersection of large language models (LLMs) and biomedicine. In particular, Vivek is the lead researcher behind Med-PaLM and Med-PaLM 2, which were the first AI systems to obtain passing and expert level scores on US Medical License exam questions respectively. Med-PaLM was recently published in Nature and has been featured in The Scientific American, Wall Street Journal, The Economist, among many others. More recently, Vivek also led the development of Med-PaLM M, the first demonstration of a generalist biomedical AI system and AMIE, a research AI system, which surpassed Primary Care Physicians on multiple axes pertaining to diagnostic dialogue in an randomized study conducted in the style of a virtual Objective Structured Clinical Examination (OSCE). Over the years, Vivek's research has been published in well-regarded journals and conferences like Nature, Nature Medicine, Nature Biomedical Engineering, JMLR, CVPR, and NeurIPS. It also forms the basis for several regulated medical device products under clinical trials at Google, including the NHS AI award winning breast cancer detection system Mammo Reader and the skin condition classification system DermAssist.

Prashant Natarajan Prashant Natarajan is a seasoned AI specialist, currently serving as the Vice President at H2O.ai and author of the book “Demystifying AI for the Enterprise.” With a diverse background in chemical engineering, linguistics, and cognitive psychology, Prashant brings a unique perspective to the world of AI and its implications for businesses and society....

The partner at investment firm Mobility Impact Partners explains how she looks beyond transportation-tech hype when investing and details a viable path for electrification through charging and infrastructure uncertainty.

From our author Dhivakar - Thiravadesam audio is available through Apple Aurality Spotify and Storytel Apps. Here the audio chapter one of Thiravadesam (this is small part of chapter) The first episode of 'Dravadesham' series. A small piece of piece! Natarajan is Natu: The captain who was called 'Nattan' came slowly. She jumped straight from the vehicle to the floor eagerly towards him. The one who saw the one who came welcomed me to see anger in his voice. "Is this how they shout out 'Nattan' for everyone to ask? How many times have I told you to call 'Natraj'.. Look that station manager looks at me like" She never cared about that station manager. But she gets angry too. Oops.. Shouldn't you be named and called Athan? Okay let it be.. First of all, take the cigarette tin out of your packet of shirt and throw it away.. Put the band in the pocket.. Father will scream when he sees. Already on a day and a half journey. ” ”Oh.. Thanks Kalyani! 'Giggled a smiling laugh and took a cigarette tin out of his top pocket and entered the band pocket with the same hurry. She stared and turned her face and waited for her dad. He just convinced the person who seemed to spread anger on his face. "Okay, why did Kalyani get angry.. Everything can be kept at home. There is no dust in the eyes during the train journey! ” 'Wow.. Thanks a lot Mr. Natraj for your care and your care.. Sorry, Captain Natraj! ” She just turned her face and replied without showing her full face and not reducing the irritation in her voice, both of them went near him knowing her father was getting down from the train. Station manager introduces himself as a gentle smile. No emotion on his face though. How much important vehicle is this Howrah mail. Won't you buy by fighting by looking at some good wooden boxes.. The hole cart.. Heavy rain from Naduvule Ongole station to Nellore.. Just flowing. If my box is like this, the other beds would be very bad. ” "Sorry sir! We are also trying. Good good passengers have sent the boxes to Europe as African.. Talked too much.. This is war season.. Order coming from Delhi before packing the existing vehicles.. ” "That is also right.. What will you do.. Which place.. Is it a magician? ” "Sir.. How did you find out sir. Yes, Mayavaram side is good.. ' "Snake's foot and snake.. Tanjavur man will put the truth about tuck tuck and break it.. Gotta be careful with him.. Hey plant.. The vehicle has been told to come to the Waltex road itself" Whether Natarajan's anger is valid to Kalyani or not, he knows that it will not happen to his uncle. He held his hand and made him sit in the cement seat. "Yes.. Let all this stuff get down.. Is Ganesha uncle inside?. When he gets down, he can take everything and get down. ” Kalyani deliberately interrupted. She called her name by pressure. "The plantation has changed a lot.. Let's go to Vizac.. All the collector and board chairman there honored us with beautiful bouquets of flowers.. Do you remember.. But your son-in-law doesn't have a bouquet of flowers.. Something else.. ” Natarajan looked at her again a little angry. But he realized in a moment that anger doesn't help and turned that look into begging. She showed beauty as different. Another voice heard from the train box to follow this fun. “Hey plant.. Are you looking good? ' Ganesan spotted near railway door.. Distance relationship between him and his uncle. Old man jumped down from the train door like a young bull folding his whore without diminishing excitement. Kalyani laughed with satisfaction after hearing the word Nattu. Even though her fake smile was bitter, the person who put a smile on his face nicely. Plant like this in front of everyone in the foreign world.. The question that when they are going to stop calling Bolt is what a question raises in his mind. But Kalyani never left him. https://youtu.be/mvXRHXJA7yU?feature=shared

Growing up in a multilingual community, Prem Natarajan became interested in language at a young age. Eventually that interest, aptitude, and curiosity translated into an interest in machine learning and technical development, and today Prem works as the chief scientist and head of enterprise AI at financial services company Capital One. Prem joins this episode to share how Capital One's technology teams are delivering value to customers by applying artificial intelligence in areas like fraud detection, how generative AI's strengths stand to transform the developer experience, and why the right combination of product, science, and engineering expertise is key to successful AI and machine learning initiatives. Read the episode transcript here. Guest bio: As chief scientist and head of enterprise AI at Capital One, Prem Natarajan leads technology strategy, architecture, and development for the company's enterprise data, analytics, and AI and machine learning initiatives, including advancing its AI capabilities, tools, and research efforts. Natarajan has more than two decades of experience leading science, technology, and commercialization efforts in natural language processing, speech recognition, computer vision, forecasting, and other applications of machine learning.  Me, Myself, and AI is a collaborative podcast from MIT Sloan Management Review and Boston Consulting Group and is hosted by Sam Ransbotham and Shervin Khodabandeh. Our engineer is David Lishansky, and the coordinating producers are Allison Ryder and Sophie Rüdinger. Stay in touch with us by joining our LinkedIn group, AI for Leaders at mitsmr.com/AIforLeaders or by following Me, Myself, and AI on LinkedIn. We encourage you to rate and review our show. Your comments may be used in Me, Myself, and AI materials.

As we approach the end of a calendar year, many of us have the practice of looking back on the year that was, reflecting on the highs and lows of the year - and shape our dreams and aspirations for the coming year.At Software People Stories, we are running a special series of conversations with people on their own approaches as well as practices and stories of how their thinking has changed over the years.Today, I am in conversation with Anantha Natarajan, my colleague from PM Power and an accomplished coach. He prefers to be called Anand.In this conversation he sharesHow his approach has evolved over the years, influenced by the context and environment he grew up in and moving to a larger city for studies and on to professional lifeA question he was asked by one of his mentors, about 25 years ago, about his aspirations for the futureHis practice of writing things down in his dream bookA model that has evolved and worked for him, that he calls i-fi; moving from the present I, to the future IThe importance of the role of a mentorWhether discipline is essential for these resolutionsHow considering some responsibilities as chores, obligations or blessings changes ones complete perspectiveThe high level overview of his i-fi modelAbout improving the quality of the inner mirrorThe relevance of choosing timelines for future plansFor more details on the i-fi model, check out Anand's blog post.Accessible at: https://pm-powerconsulting.com/blog/i-fi-a-model-for-designing-your-future-and-personal-change/I hope you got some ideas to help you reflect and plan for the coming year.If some other practices have worked for you - or possibly not worked for you, would you like to share your story?Reach us on podcasts@pm-powerconsulting.com  and please do share with your networks to spread the word.

Today we're joined by Prem Natarajan, chief scientist and head of enterprise AI at Capital One. In our conversation, we discuss AI access and inclusivity as technical challenges and explore some of Prem and his team's multidisciplinary approaches to tackling these complexities. We dive into the issues of bias, dealing with class imbalances, and the integration of various research initiatives to achieve additive results. Prem also shares his team's work on foundation models for financial data curation, highlighting the importance of data quality and the use of federated learning, and emphasizing the impact these factors have on the model performance and reliability in critical applications like fraud detection. Lastly, Prem shares his overall approach to tackling AI research in the context of a banking enterprise, including prioritizing mission-inspired research aiming to deliver tangible benefits to customers and the broader community, investing in diverse talent and the best infrastructure, and forging strategic partnerships with a variety of academic labs. The complete show notes for this episode can be found at twimlai.com/go/658.

COP27: Loss and Damage Funds to Combat Climate Change (Interview with Prof. Usha Natarajan) by Inter Gentes

Tara sits down with Mahesh Natarajan, COO of the leading destination spa resort Ananda in the Himalayas, to explore insights from one of the premiere getaways for physical, emotional, and spiritual transformation. They also discuss Ananda's specialties: ancient Indian philosophies combined with expert-led yoga, ayurveda, breathwork, meditation, and other international wellness therapies.Follow Ananda in the Himalayas on Social Media:Instagram: https://www.instagram.com/anandainthehimalayasFacebook: https://www.facebook.com/AnandaInTheHimalayasYouTube: https://www.youtube.com/channel/UCdjArurztFUg2YoqCvsjBwQ-----Visit Ananda in the Himalayas Website: https://www.anandaspa.com/-----Follow Dr. Tara on Social Media:Instagram: https://www.instagram.com/drtaraswartTwitter: https://twitter.com/TaraSwartLinkedIn: https://www.linkedin.com/in/taraswartTikTok: https://www.tiktok.com/@drtaraswart

In this episode of Medsider Radio, we sat down with Shyam Natarajan, founder and CEO of Avenda Health, which utilizes artificial intelligence and cutting-edge imaging to improve the diagnosis and treatment of prostate cancer.After getting his PhD in Biomedical Engineering from UCLA, Shyam worked as a postdoctoral scholar in UCLA's Department of Surgery, focusing on minimally invasive surgical interventions. He also managed the UCLA Business of Science Center, spearheading initiatives to guide students toward non-academic career paths. With experiences like founding UCLA Innovation Week and the Inventathon, he is committed to pushing the boundaries of medical technology. At Avenda Health, Shyam is now leading the charge in revolutionizing prostate cancer care. In this interview, we talk about what it really takes to understand the market need for your product or service, how prototypes can be incredibly helpful in convincing relevant parties, how Shyam approaches fundraising, and what to expect from medtech in the future given current technological advancements in growing fields like AI. Before we dive into the discussion, I wanted to mention a few things:First, if you're into learning from medical device and health technology founders and CEOs, and want to know when new interviews are live, head over to Medsider.com and sign up for our free newsletter.Second, if you want to peek behind the curtain of the world's most successful startups, you should consider a Medsider premium membership. You'll learn the strategies and tactics that founders and CEOs use to build and grow companies like Silk Road Medical, AliveCor, Shockwave Medical, and hundreds more!We recently introduced some fantastic additions exclusively for Medsider premium members, including playbooks, which are curated collections of our top Medsider interviews on key topics like capital fundraising and risk mitigation, and a curated investor database to help you discover your next medical device or health technology investor!In addition to the entire back catalog of Medsider interviews over the past decade, premium members also get a copy of every volume of Medsider Mentors at no additional cost, including the recently launched Medsider Mentors Volume IV. If you're interested, go to medsider.com/subscribe to learn more.Lastly, if you'd rather read than listen, here's a link to the full interview with Shyam Natarajan.

What's in your fintech blueprint?Wait, you say, what's a fintech blueprint? Good question and if you didn't ask it probably you should have because few credit unions have current blueprints or even old, dusty ones.On that note, how often should you update a fintech blueprint? On the show today is  Prakash Natarajan, managing director for payments strategy for SRM and he says every three years. Ask me and I'd say every two years.Either way the point is that the fintech landscape is fast morphing - who knew about generative AI 9 months ago - and an institution needs a blueprint that sets out fintech priorities and why they matter.Otherwise you are at the mercy of the next fintech sales person in your office who waves a shiny object in your face and, yep, it's cool…but do your members and institution really have to have it? That is why you need a blueprint.Background reading for this show is the SRM report Why Every Financial Institution Needs a Fintech Blueprint. It's free, click hereListen up.Like what you are hearing? Find out how you can help sponsor this podcast here. Very affordable sponsorship packages are available. Email rjmcgarvey@gmail.com  And like this podcast on whatever service you use to stream it. That matters.  Find out more about CU2.0 and the digital transformation of credit unions here. It's a journey every credit union needs to take. Pronto

In this episode, Nathan sits down with Vivek Natarajan and Tao Tu of Google's Med-PaLM, diving into how they used one of the world's largest medical datasets ever compiled to develop Med-PaLM M, an AI agent specialized in medical tasks. In this episode, they discuss: Med-PaLM M's “clinically superhuman” abilities and limitations, the rigorous testing and validation that went into the model, and their vision for AI to take over repetitive clerical tasks and allow doctors to focus on patients. RECOMMENDED PODCAST: The HR industry is at a crossroads. What will it take to construct the next generation of incredible businesses – and where can people leaders have the most business impact? Hosts Nolan Church and Kelli Dragovich have been through it all, the highs and the lows – IPOs, layoffs, executive turnover, board meetings, culture changes, and more. With a lineup of industry vets and experts, Nolan and Kelli break down the nitty-gritty details, trade offs, and dynamics of constructing high performing companies. Through unfiltered conversations that can only happen between seasoned practitioners, Kelli and Nolan dive deep into the kind of leadership-level strategy that often happens behind closed doors. Check out the first episode with the architect of Netflix's culture deck Patty McCord. https://link.chtbl.com/hrheretics TIMESTAMPS: (00:00) Episode Preview (00:00:56) Introducing Vivek Natarajan and Tao Tu (00:04:18) The story of Google's Medical AI research progress (00:07:11) Multi-modal Med-PaLM (00:10:32) Genomic data - how do you represent it? (00:11:13) Google's Deep Variant (00:14:44) The successes and failures behind the incredible pace of progress (00:15:02) Sponsors: Netsuite | Omneky (00:21:54) Google's research culture and assembling an interdisciplinary team (00:31:36) Google's Pathways (00:33:40) Med-PaLM M's architecture (00:37:28) Working with 3 different model sizes and what you learn (00:46:56) Data and compute required for Med-PaLM M (00:49:38) Med-PaLM M's cycle time (00:54:56) Is a bridge or adapter structure worth implementing? (01:00:09) Can we create an AI doctor? (01:02:39) Emergent capabilities like identifying tuberculosis (01:09:37) Reactions to these emergent capabilities (01:11:13) Moving towards clinical trials and real-world testing (01:13:01) Regulatory and safety considerations (01:15:03) AI safety in the healthcare domain (01:17:00) Potential to transform healthcare access worldwide LINKS: Med-PaLM: https://sites.research.google/med-palm/ Med-PaLM M paper: https://arxiv.org/abs/2307.14334 Our earlier conversation with Vivek Natarajan on Med-PaLM: https://www.youtube.com/watch?v=nPBd7i5tnEE X/TWITTER: @vivnat (Vivek) @taotu831 (Tao) @labenz (Nathan) @eriktorenberg @CogRev_Podcast SPONSORS: NetSuite | Omneky NetSuite has 25 years of providing financial software for all your business needs. More than 36,000 businesses have already upgraded to NetSuite by Oracle, gaining visibility and control over their financials, inventory, HR, eCommerce, and more. If you're looking for an ERP platform ✅ head to NetSuite: http://netsuite.com/cognitive and download your own customized KPI checklist. Omneky is an omnichannel creative generation platform that lets you launch hundreds of thousands of ad iterations that actually work customized across all platforms, with a click of a button. Omneky combines generative AI and real-time advertising data. Mention "Cog Rev" for 10% off.

Today, we're excited to get to know Vivek, AI researcher at Google and one of the lead researchers for Med-PaLM2, and Viswesh, CTO and Founder of Valar Labs! Vivek is a Research Scientist at Google Health AI advancing biomedical AI to help scale world class healthcare to everyone. Vivek is particularly interested in building large language models and multimodal foundation models for biomedical applications and leads the Google Brain moonshot behind Med-PaLM, Google's flagship medical large language model. Med-PaLM has been featured in publications such as The Scientific American and Forbes. Vivek graduated with his masters from UT Austin in Computer Science and Bachelors at National Institute of Technology in India. Viswesh is the CTO and Co-Founder of Valar Labs. Valar Labs is building clinical grade deep learning to analyze each patient's characteristics and provide clarity to oncologists during decision making. Their AI is built with oncologists at the center and provides interpretable and actionable insights. Prior to founding Valar Labs, Viswesh was a Research Assistant in Stanford's Artificial Intelligence Laboratory (SAIL) leveraging cutting edge artificial intelligence to solve healthcare problems. He was also the founder of Kanna, a patented and clinically-validated method to detect Amblyopia in children in India. Viswesh graduated with a bachelors in Computer Science at Stanford. In this episode, Vivek and Viswesh shares how they got into Healthcare AI research and how they fell into different career paths, one leading Research at Google Health AI and the other as the CTO and Co-Founder of Valar Labs. We talk about the future of LLMs in healthcare, and also how to build defensibility in AI healthcare startups.

Viji Natarajan is a pioneering expert in Women's Health and the Founder and Chief Ayurvedic Officer of Divine Journey, an International Wellness Company that provides deep, therapeutic healing to the women of the world. Using a blend of ancient healing practices and wisdom rooted in Ayurvedic Medicine integrated with evidence based practices in neuroscience, pharmacology and genetics, she helps women throughout the entire arc of their life and reproductive journey. In this episode, you will learn the following: Ayurvedic Medicine is the utmost epitome of Personalized medicine and can be used to create health every day. Understand that mental health, physical health and spiritual health are no longer a choice. It is a priority in order to be healthy, happy and thrive. We as women must prioritize our own health. Contact Viji Natarajan: Email: info@divinejourney.me Website: www.divinejourney.me Instagram: https://www.instagram.com/divinejourneyllc/ LinkedIn: https://www.linkedin.com/in/divinejourney108/ Facebook: https://www.facebook.com/search/top?q=%40divinejourney108 Contact Dr. Mary: Email: mary@drmarysanders.com Website: www.drmarysanders.com Instagram: https://www.instagram.com/dr.maryesanders/ Facebook: https://www.facebook.com/dr.maryesanders LinkedIn: https://www.linkedin.com/in/drmaryesanders/

Sriraam Natarajan is a Professor of Computer Science and Director of the Center for Machine Learning at The University of Texas at Dallas. In this episode Dr. Natarajan speaks with Pitt HexAI's podcast host Jordan Gass-Poore' about his background and interests in artificial intelligence and machine learning with a focus on healthcare and biomedical applications. Sriraam and Jordan discuss work being carried out at the University of Texas, advice Dr. Natarajan commonly offers students, his being chosen to chair the Association for the Advancement of Artificial Intelligence's upcoming AAAI-24 conference and his views on explainable AI.

Pari Natarajan is the CEO of Zinnov, a global management and consulting firm with core expertise in globalization, product engineering and digital transformation.In this episode, we talk about the evolution of digital transformation 1.0 to digital transformation 2.0, the current phase we're in now. We break down the concepts of digital plumbing and integrated experience, then discuss the role of sustainability in the future of digital transformation before concluding with some predictions for the future of automotive and entertainment.Links & mentions:zinnov.comlinkedin.com/in/parinatarajanzinnov

 https://www.groupbyinc.com/news/news-articles/groupby-delivers-next-gen-ecommerce-search.Arv's LinkedIn, https://www.linkedin.com/in/arvnatarajan/?originalSubdomain=caGroupBy's LinkedIn, https://www.linkedin.com/company/groupby-inc/Twitter, https://twitter.com/GroupByInc

Nathan sits down with Vivek Natarajan, research scientist at Google Health. Vivek leads the Google Brain moonshot behind Med-PaLM, Google's flagship medical large language model, featured in The Economist, The Scientific American, CNBC, and Forbes. In this episode, they discuss the foundational models that Vivek and team built before Med-PaLM, the techniques used to develop Med-PaLM which will be of interest to anyone developing AI systems for high-stakes use cases, and the capabilities for Med-PaLM to equalize access to medical knowledge and care. This episode is part of a series centered on talking to the people at the cutting edge of building AI-driven solutions in medicine. RECOMMENDED PODCAST: The HR industry is at a crossroads. What will it take to construct the next generation of incredible businesses – and where can people leaders have the most business impact? Hosts Nolan Church and Kelli Dragovich have been through it all, the highs and the lows – IPOs, layoffs, executive turnover, board meetings, culture changes, and more. With a lineup of industry vets and experts, Nolan and Kelli break down the nitty-gritty details, trade offs, and dynamics of constructing high performing companies. Through unfiltered conversations that can only happen between seasoned practitioners, Kelli and Nolan dive deep into the kind of leadership-level strategy that often happens behind closed doors. Check out the first episode with the architect of Netflix's culture deck Patty McCord. https://link.chtbl.com/hrheretics LINKS: https://sites.research.google/med-palm/ FEEDBACK / COLLABORATE WITH NATHAN: Email: TCR@turpentine.co TIMESTAMPS: (00:00) Episode preview (03:43) The story of how Med-PaLM came to be (09:41) Building Med-PaLM's infrastructure (13:10) The US medical licensing exam as a measure of AI progress (15:23) Sponsor: Omneky (18:17) Practicality of benchmarking in real-world usage (21:39) Overcoming the shortfalls of Flan-PaLM with Med-PaLM (25:08) Choosing to use soft prompting over few shot prompting (30:36) The process of training Flan-PaLM (37:31) A curriculum approach to soft-prompting (38:43) Layperson vs expert interactions with LLMs (43:54) How did the Google team facilitate user exploration of the model's capabilities? (46:58) Shift in techniques from Med-PaLM to Med-PaLM2 (50:21) Using different prompting strategies with Med-PaLM2 (57:33) Is Med-PaLM 2 preferred over clinicians? (01:02:28) Will there be a multimodal version of Med-PaLM? (01:04:52) Breakthroughs required for AI to further advance human potential (01:10:23) The Med-PaLM business plan (01:12:08) Is there a vision for a consumer product? (01:15:46) The pros and cons of pre-training a model (01:19:45) Vivek's favorite AI products (01:21:01) Would Vivek get a Neuralink implant? (01:23:08) AI hopes and fears TWITTER: @CogRev_Podcast @vivnat (Vivek) @labenz (Nathan) @eriktorenberg (Erik) Thank you Omneky for sponsoring The Cognitive Revolution. Omneky is an omnichannel creative generation platform that lets you launch hundreds of thousands of ad iterations that actually work, customized across all platforms, with a click of a button. Omneky combines generative AI and real-time advertising data. Mention "Cog Rev" for 10% off. Music Credit: MusicLM More show notes and reading material released in our Substack: https://cognitiverevolution.substack.com/

Dr. Bouchard discusses " Familial Hypercholesterolemia" with Dr. Pradeep Natarajan from Harvard.

S2E17: Informed Skepticism for ChatGPT with Prashant Natarajan, General Manager at H2O.ai and host Dr. Nick. What Does ChatGPT Mean for Healthcare? Continuing the series on ChatGPT with best selling author of Demystifying AI for the Enterprise. Are we at a critical inflection point and expecting to see a big acceleration in automation and insights generated from semi-intelligent systems that generate newfound understanding in healthcare. And for now its clear, ChatGPT is not the advent of Skynet from Terminator but rather the launch of the first rocket on our journey into interstellar space. This an early but critical step on the way to the incredible progress that can automate many of our mundane tasks and elevate data to knowledge that we can use more effectively in healthcare. Your better pill to swallow is to accept the arrival of augmented, assisted intelligence that can deliver real value in healthcare making use of the huge data lakes being created in many areas by linking the data to value propositions in your setting. The capabilities are available but tend to be narrow and not generalizable But as I said with speech recognition many years ago – you are either on the train, in this case, the AI train or you are on the platform watching the train leave. To stream our Station live 24/7 visit www.HealthcareNOWRadio.com or ask your Smart Device to “….Play Healthcare NOW Radio.” Find all of our network podcasts on your favorite podcast platforms and be sure to subscribe and like us. Learn more at www.healthcarenowradio.com/listen

It's beautiful to see my fellow South Asian women creating safe spaces for people for women who have often felt like they don't belong . My guest Aasheekaa Natarajan has made it her mission to  help women get unstuck, get out of their own way, and ignite their SPARK. Super excited to share that if you are looking for a new container for you to learn and grow in — then check out Aasheekaa's newest LIVE group program with tons of built-in support. Learn more here. Next round begins March 28, 2023!Follow and connect with Aasheekaa on Instagram here! Support the showSUPPORT THE SHOW ORDER MY NEW BOOK, Say It Out Loud—PRE-ORDER TODAY APPLY to work privately with Vasavi—Learn more JOIN the Say It Out Loud Safe Haven Community!—Learn more FOLLOW Vasavi Kumar on IG

Welcome to the Tearsheet Podcast. I'm Tearsheet editor in chief, Zack Miller. An interesting thing is starting to happen with partner banks. What began as the purview of some smaller, regional players is now becoming interesting to some of the largest global banks. For example, we spoke a couple of weeks ago to Citi about its plans to provide partner bank services for global firms. That means a brand or fintech with global aspirations could work with a single bank in each market, instead of partnering with different local players on the ground. Standard Chartered is already supporting its clients with its own extensive footprint in Asia, Africa, and the Middle East. I spoke with Anand Natarajan, who covers the technology, media and fintech segments for the firm's treasury services. At a conversation that began in Las Vegas in 2022 and continued into the beginning of 2023, Anand shares his view on a wide range of topics including evolving merchant ecommerce experiences, social commerce, gaming payments, CBDCs and more. It was an engaging conversation – hope you enjoy it. Here's my talk with Anand Natarajan.

Live from Manifest The Future of Logistics Conference In Las Vegas, Omni Talk Retail's Anne Mezzenga and Chris Walton sit down with a man who is known now by one name, and that is Quiet Platform's President, Shekar. Shekar kicked off the Manifest conference as the keynote speaker and then joined Chris and Anne to explain the goals of Quiet Platforms, how they are different from a traditional 3PL, and the power that is possible if retailers become "Frenemys." Thanks to Harbor Lockers By Luxer One For making this content possible. You can find out more by going to https://harborlockers.com/ Music by HookSounds.com

Today we are visiting the Himalayan region of India, birthplace of Yoga and Ayurveda, and famed location of the ashrams visited by The Beatles and in Eat Pray Love.  My guest today is Mahesh Natarajan, the COO of Ananda, a destination spa resort set in the foothills of the Himalayas. Ananda is one of those rare places where you can experience both total physical and spiritual transformation while enjoying a luxurious setting.  In addition to deep wellness and spa experiences, Ananda is also a great jumping off spot to explore the region. Mahesh and I chat about everything from the core principles of Ayurveda to art, and local culture.  Thank you to our sponsor for this episode, Covac Global.   Learn more at www.luxtravelinsider.com   Connect with me on Social: Instagram LinkedIn

As the burden of cardiovascular disease increases in the United States, the importance of enhanced screening tools, early risk prediction, and prevention strategies grows. Novel risk scoring methods, including polygenic risk scores (PRS), may help identify patients that benefit from early intervention and risk modification. In this episode, we discuss how a PRS is calculated, how to incorporate a PRS into clinical practice, and current barriers to the equitable implementation of risk scores. In terms of frontiers in clinical genetics we also discuss the burgeoning field of pharmacogenetics and how pharmacogenetics may be used to identify responders and non-responders to certain therapies. Join CardioNerds Dr. Jessie Holtzman (CardioNerds Academy Chief and Chief Resident and soon FIT at UCSF), Dr. Alaa Diab (CardioNerds Academy Fellow and Medicine Resident at GBMC), and student doctor Hirsh Elhence (CardioNerds Academy Intern and medical student at USC Keck School of Medicine) as they discuss frontiers in clinical genetics with Dr. Pradeep Natarajan (Director of Preventive Cardiology, Massachusetts General Hospital). Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig. This episode was developed in collaboration with the American Society of Preventive Cardiology and is supported with unrestricted educational funds from Illumina, Inc. All CardioNerds content is planned, produced, and reviewed solely by CardioNerds. This CardioNerds Cardiovascular Genomics series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs. Pearls • Notes • References CardioNerds Cardiovascular Genomics PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - Frontiers in Clinical Genetics in Cardiovascular Prevention For common diseases like coronary artery disease, rare mutations may confer a several-fold increased risk of disease – for instance, in familial hypercholesterolemia, a single rare mutation may confer as much as a three-fold increase in risk of coronary artery disease. However, for most common diseases, the overall cumulative impact of several common genetic variants may be greater than that of a monogenetic trait. Family history is a particularly coarse predictor of CV risk, highlighting the need for polygenic risk scores. In particular, younger patients with borderline cardiovascular risk may benefit from the use of a polygenic risk score in the determination of their overall cardiovascular risk profile. A polygenic risk score (PRS) is a weighted sum of several risk-conferring alleles. The weight assigned to an allele is determined by the strength of the association between the allele and CV disease, as determined by genome-wide association studies (GWAS). The data used for genome-wide associated studies in cardiovascular disease have historically included populations primarily of European ancestry. However, more data is being collected from diverse patient cohorts to increase the external validity and broader applicability of such studies. Pharmacogenetic polygenic risk scores may be used to predict drug efficacy and toxicity, as well as to identify biologically plausible drug targets for clinical trial design. Show notes - Frontiers in Clinical Genetics in Cardiovascular Prevention What is a polygenic risk score (PRS)? Monogenic conditions are those in which a variant in a single gene causes a pathological phenotype. For example, familial hypercholesterolemia is often the result of a mutated allele in the LDL receptor gene. In contrast, polygenic risk suggests that there are variants in multiple genes that all confer risk independently, each with a small individual effect size. By aggregating many variants,

During the pandemic, the way you've eaten has likely changed. Either you ate out less, you cooked more, or you wholeheartedly embraced food delivery such as DoorDash, Deliveroo, Grab, Swiggy or Zomato based on where you live.The Food Service industry was worth over $900B in 2021 just in North America and it's only getting bigger. It's also changing.. you may have experienced it already - with all sorts of new experiences, like food delivery, home chefs, and even robot-made food!As robots become more and more complex, the tasks they're able to complete is growing! Roomba's can clean your house, mow your lawn, The Da Vinci robot by Intuitive aids in surgeries and we haven't even touched on the scale of robotics in manufacturing industries.So what about a robot that makes you a meal?Today, on Things Have Changed, we chat with Rajagopal (Raja) Natarajan, CEO & Co-Founder of Xook, to talk about how his team are pioneering a different type of food experience which involves sophisticated robotics, software and some very delicious meals.One day soon, a robot will make you a salad. And it might just be a Xook machine